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Neuroplasticity

Neuroplasticity, also known as neural plasticity or brain plasticity, refers to the ability of the nervous system to change its activity in response to intrinsic or extrinsic stimuli by reorganizing its structure, functions, or connections after experiences such as learning, injury, or environmental changes.^[1] This dynamic process enables the brain to adapt throughout life, forming the basis for skill acquisition, memory formation, and recovery from neurological damage.^[2] Historically, the concept of plasticity was first referenced by William James in 1890, with the term "neural plasticity" coined by Jerzy Konorski in 1948 and further popularized by Donald Hebb's 1949 work on synaptic strengthening.^[1] Key mechanisms include synaptic plasticity, such as long-term potentiation (LTP) and long-term depression (LTD), which adjust the strength of neural connections; structural changes like dendritic spine remodeling and collateral sprouting; and adult neurogenesis, particularly in the hippocampus and olfactory bulb, though its extent in humans remains debated.^[1]^[2] Factors influencing neuroplasticity encompass exercise, enriched environments, neuromodulators like dopamine and brain-derived neurotrophic factor (BDNF), and repetition, while aging and neurodegenerative diseases can impair it through reduced synaptic efficiency and neurogenesis.^[1]^[2] Across the lifespan, neuroplasticity is most pronounced during early development, where critical periods allow rapid adaptation to sensory inputs, and persists into adulthood for learning and habit formation, though it declines with age due to factors like brain atrophy and diminished BDNF levels.^[2] In disease contexts, it facilitates recovery from stroke or traumatic brain injury via functional reorganization, such as vicariation where undamaged areas assume lost functions, but can also lead to maladaptive outcomes like chronic pain or phantom limb sensations.^[1] Therapeutic interventions, including constraint-induced movement therapy, mirror therapy, and pharmacological agents like selective serotonin reuptake inhibitors (SSRIs), harness neuroplasticity to enhance rehabilitation, with recent evidence showing exercise increases hippocampal volume and cognitive function in older adults.^[1]^[2]

Historical Development

Origin of the Concept

The notion of the brain's adaptability to injury or experience originated in ancient philosophical and medical thought. Galen (c. 129–216 AD), a Roman physician and anatomist, advanced early ideas on brain resilience by describing the organ's "twinned" ventricular structure, which he believed enabled compensatory function following damage, such as sustaining sensory and motor capabilities after localized lesions.^[1] This concept prefigured later discussions of equipotentiality, implying the brain's inherent capacity to redistribute functions rather than being rigidly fixed. Hippocrates (c. 460–370 BC) emphasized the brain as the seat of intelligence and documented recovery from head injuries through empirical observation and treatment.^[3] In the 19th century, scientific debates sharpened the contrast between strict localizationism—positing fixed brain regions for specific functions—and holistic views of cerebral equipotentiality. Pierre Flourens (1794–1867), a French physiologist, challenged localizationist theories advanced by Franz Joseph Gall by conducting ablation experiments on pigeons and frogs, concluding that the brain operated as an integrated whole where higher functions were diffusely distributed rather than confined to discrete areas.^[4] Flourens' doctrine of equipotentiality argued that lesions disrupted overall performance proportionally to their size, not location, laying groundwork for understanding adaptive reorganization. These ideas influenced subsequent work, including Karl Lashley's early 20th-century extension through rat lesion studies, which formalized equipotentiality and mass action principles: the former suggesting any intact cortical area could assume lost functions, and the latter proposing that behavioral deficits scaled with lesion extent across the cortex, not specificity.^[5] The term "plasticity" entered neuroscience lexicon in 1890 with William James, who in The Principles of Psychology described the nervous system's "plasticity" as its tendency to form enduring modifications in neural pathways through habit formation and experience, enabling behavioral adaptation.^[5] This marked a shift from anatomical rigidity to modifiable connectivity. In the late 19th and early 20th centuries, Santiago Ramón y Cajal advanced concepts of neuronal plasticity by investigating degeneration, regeneration, and adaptive changes in neural structures, laying foundational ideas for modifiable neural connections.^[6] Similarly, Adolf Meyer in 1902 referred to the nervous system as the "apparatus of biological plasticity," emphasizing its capacity for change throughout life.^[7] By the mid-20th century, the concept evolved amid growing evidence from animal studies challenging fixed brain doctrines. In the 1940s, lesion experiments by Margaret A. Kennard on infant monkeys demonstrated superior motor recovery compared to adults after cortical removals, attributing outcomes to age-dependent plasticity and prompting a reevaluation of the brain's developmental flexibility.^[8] Concurrently, Jerzy Konorski coined "neural plasticity" in 1948 to denote experience-driven changes, a term popularized by Donald Hebb's 1949 The Organization of Behavior, which proposed synaptic strengthening as a mechanism for learning and recovery, resurrecting and refining earlier synaptic theories after Lashley's critiques.^[1] These developments signified a pivotal transition from static to dynamic models of brain function.

Key Discoveries and Researchers

The 1960s saw a revival of research into brain plasticity, spurred by Vernon Mountcastle's 1957 discovery of the columnar organization of the neocortex through microelectrode recordings in cat somatosensory cortex, which revealed vertically oriented functional units responsive to specific sensory modalities and suggesting a modular, adaptable brain architecture.^[9] Karl Lashley's extensive engram studies from the 1920s to the 1950s, using controlled lesions in rats and monkeys trained on maze tasks, provided early empirical challenges to the idea of fixed localization for learning and memory.^[10] He found that memory performance degraded more with the overall size of cortical damage than with its precise location, leading to his principles of mass action and equipotentiality, where functions are distributed across broad regions rather than confined to discrete sites.^[11] In his influential 1950 summary, Lashley concluded that the engram—the physical trace of memory—could not be isolated to specific loci, implying a dynamic, non-static neural basis for cognition.^[12] David Hubel and Torsten Wiesel advanced understanding of developmental plasticity through their 1960s and 1970s experiments on the visual cortex of kittens and monkeys, mapping receptive fields and identifying ocular dominance columns as alternating strips driven preferentially by each eye.^[13] Their work demonstrated critical periods in early life, during which monocular deprivation caused lasting shifts in cortical dominance toward the open eye, with columns failing to segregate properly and leading to amblyopia-like deficits. These findings, which highlighted experience-dependent wiring of the visual system, earned Hubel and Wiesel the 1981 Nobel Prize in Physiology or Medicine, shared with Roger Sperry. Michael Merzenich's research in the 1970s and 1980s on adult owl monkeys established plasticity beyond development, showing rapid remapping in the somatosensory cortex (area 3b) after peripheral manipulations like digit amputation or nerve section.^[14] In one key study, microelectrode recordings 2–8 months post-amputation revealed that the cortical territory formerly devoted to the removed digit was invaded by representations of adjacent fingers and palm, demonstrating adaptive reorganization driven by behavioral use.^[15] This work underscored that adult brains retain substantial capacity for functional redistribution in response to injury or altered input. Paul Bach-y-Rita's innovations from the 1960s onward introduced sensory substitution devices, leveraging plasticity to restore perceptual functions in sensory-impaired individuals through cross-modal adaptation.^[16] His pioneering 1969 system used a closed-circuit television camera to convert visual scenes into tactile patterns delivered via a 400-vibrator array on the subject's back, allowing blind users to discriminate shapes, directions, and distances after brief training, thus evidencing the brain's ability to reassign sensory processing pathways for rehabilitation.^[17]

Neurobiological Foundations

Structural Changes

Structural neuroplasticity encompasses the physical modifications in the brain's neural architecture that support adaptive changes, including alterations in neuron morphology such as the formation of new dendritic spines and the process of synaptogenesis.^[2] Dendritic spines, small protrusions on neuronal dendrites, serve as primary sites for excitatory synapses and undergo dynamic remodeling to facilitate these changes.^[18] Synaptogenesis involves the creation of new synaptic connections between neurons, enabling the expansion of neural circuits in response to experience or injury.^[19] Key processes underlying structural neuroplasticity include long-term potentiation (LTP), which not only strengthens synaptic efficacy but also induces lasting morphological alterations like synapse enlargement and stabilization.^[20] LTP triggers the selective clustering and long-term stabilization of synapses.^[21] Additionally, axonal sprouting allows for the growth of new axonal branches, facilitating the rewiring of neural pathways by forming novel connections with target neurons.^[2] These mechanisms collectively contribute to the brain's capacity for circuit reorganization without the need for new neuron generation in most regions. Evidence from neuroimaging supports these structural shifts, as demonstrated by magnetic resonance imaging (MRI) studies showing increases in gray matter volume following intensive learning tasks. For instance, in a seminal study, adults trained in juggling for three months exhibited transient expansions in gray matter in visual motion areas, such as the mid-temporal region and posterior intraparietal sulcus, which partially reversed after training cessation. Such findings highlight how skill acquisition can drive measurable anatomical changes in the adult brain. Structural neuroplasticity is more pronounced during juvenile development, where rapid synaptogenesis and dendritic arborization establish foundational neural networks, but it persists into adulthood under conditions of enriched stimulation or targeted training.^[22] In adults, these changes occur at a slower rate yet remain essential for adaptation, underscoring the brain's lifelong potential for morphological remodeling.^[2]

Functional Reorganization

Functional reorganization in neuroplasticity encompasses the dynamic adaptations of existing neural circuits, characterized by alterations in neural firing patterns, synaptic efficacy, and the recruitment of neural networks, enabling rapid behavioral adjustments without necessitating permanent structural changes.^[1] These changes allow the brain to redistribute functions across intact areas, compensating for disruptions such as injury or sensory loss.^[23] Unlike structural plasticity, which involves anatomical remodeling, functional reorganization operates on reversible, activity-dependent timescales to maintain or restore behavioral output.^[24] Key mechanisms underlying functional reorganization include the unmasking of dormant or ineffective synapses, which become active under altered conditions like deafferentation, thereby expanding the functional reach of neural circuits.^[25] Changes in neurotransmitter release also contribute, modulating synaptic strength through presynaptic adjustments that enhance or suppress signal transmission in response to activity patterns. Additionally, recruitment of homologous areas in the contralateral hemisphere facilitates compensation, particularly in cases of unilateral damage, where undamaged regions assume roles typically handled by the affected side.^[26] Electrophysiological studies provide clear examples of these processes, such as shifts in receptive fields following peripheral deafferentation, where neurons in the somatosensory cortex rapidly incorporate inputs from adjacent skin regions after nerve section or digit amputation.^[27] In these experiments, multi-unit recordings revealed that deprived cortical zones in area 3b of monkeys expanded their representations of neighboring digits within hours, demonstrating how functional remapping supports sensory adaptation.^[28] These adaptations occur across distinct time scales: short-term changes, manifesting in seconds to minutes, often arise from immediate unmasking of latent connections and transient excitability shifts.^[25] Medium-term reorganizations, unfolding over hours to days, involve sustained modifications in synaptic efficacy and network recruitment to consolidate behavioral recovery.^[23] Over extended periods, such functional shifts may contribute to subsequent structural changes as a long-term outcome.^[24]

Molecular and Cellular Mechanisms

At the molecular and cellular levels, neuroplasticity is driven by intricate biochemical cascades that modulate synaptic strength and neuronal connectivity. Central to these processes is brain-derived neurotrophic factor (BDNF), a neurotrophin that promotes synaptogenesis by enhancing dendritic spine density and facilitating the maturation of excitatory synapses in the hippocampus and cortex. BDNF binds to its high-affinity receptor TrkB, activating downstream signaling pathways such as MAPK/ERK and PI3K/Akt, which ultimately support the formation and stabilization of new synaptic contacts during development and in response to activity. Similarly, N-methyl-D-aspartate (NMDA) receptors play a pivotal role in long-term potentiation (LTP), a core mechanism of synaptic plasticity, by permitting calcium influx upon coincident presynaptic glutamate release and postsynaptic depolarization, thereby initiating intracellular signaling for persistent synaptic strengthening. Key cellular processes underpinning these changes involve calcium-dependent signaling that couples synaptic activity to gene expression. Following NMDA receptor activation, calcium influx elevates intracellular Ca²⁺ levels, which binds to calmodulin and activates kinases like CaMKII, leading to the phosphorylation and activation of the transcription factor CREB (cAMP response element-binding protein) at serine 133. This CREB activation promotes the transcription of plasticity-related genes, including BDNF itself and Arc, which are essential for structural remodeling and memory consolidation. Complementing these mechanisms, epigenetic modifications such as DNA methylation fine-tune the expression of plasticity genes by adding methyl groups to cytosine residues in CpG islands, often repressing transcription factors like BDNF in response to environmental cues, thereby providing a stable yet reversible layer of regulation over long-term plasticity. A foundational model for LTP induction at the synaptic level is captured by spike-timing-dependent plasticity (STDP), where synaptic weight changes depend on the relative timing of pre- and postsynaptic spikes. A simplified formulation is: For Δt > 0 (presynaptic spike precedes postsynaptic): Δw = A_+ exp(Δt / τ_+), For Δt < 0: Δw = -A_- exp(-Δt / τ_-), where Δt = t_post - t_pre, A_+ and A_- are amplitude factors for potentiation and depression, and τ_+ and τ_- are time constants. This reflects how precise temporal correlations drive bidirectional adjustments in synaptic efficacy, with potentiation (LTP-like) when the postsynaptic spike follows the presynaptic closely, and depression (LTD-like) otherwise. Recent research through 2025 has highlighted the role of microRNAs (miRNAs) in fine-tuning neuroplasticity by post-transcriptionally regulating mRNA stability and translation of synaptic proteins, such as miR-134 modulating dendritic spine morphology and miR-132 enhancing LTP via CREB pathway amplification. Additionally, inflammation modulates plasticity through cytokines like IL-1β and TNF-α, which, when elevated in neuroinflammatory states, impair LTP induction by altering NMDA receptor trafficking and promoting synaptic pruning, as evidenced in models of chronic stress and aging.

Types of Neuroplasticity

Synaptic Plasticity

Synaptic plasticity refers to the ability of synapses to strengthen or weaken over time in response to increases or decreases in their activity, serving as a fundamental mechanism for neural adaptation and information processing in the brain. This process operates at the level of individual synaptic connections between neurons, enabling dynamic modifications that underpin learning and memory. Central to synaptic plasticity is the Hebbian principle, articulated by Donald Hebb in 1949, which posits that "cells that fire together wire together." This principle describes a form of coincidence detection where the repeated synchronous activation of presynaptic and postsynaptic neurons leads to an enhancement of synaptic efficacy, as the presynaptic neuron's activity strengthens the connection only when it temporally correlates with postsynaptic firing, thereby associating active neural assemblies.^[29] The primary forms of synaptic plasticity are long-term potentiation (LTP) and long-term depression (LTD), which represent persistent increases and decreases, respectively, in synaptic strength lasting from minutes to hours or longer. LTP is typically induced by high-frequency stimulation (e.g., tetanic stimulation at 100 Hz for 1 second) of presynaptic afferents, leading to a robust, input-specific enhancement of postsynaptic responses, as first demonstrated in the hippocampal dentate gyrus of anesthetized rabbits.^[30] In contrast, LTD is elicited by low-frequency stimulation (e.g., 1 Hz for 10-15 minutes), resulting in a lasting weakening of synaptic transmission that helps refine neural circuits by reducing the influence of less active connections.^[31] Experimental evidence from in vitro studies of hippocampal slices has shown that LTP involves the trafficking of AMPA receptors to the postsynaptic membrane, where their insertion increases the amplitude of excitatory postsynaptic currents, thereby amplifying synaptic responses without altering presynaptic release probability.^[32] Synaptic plasticity remains critical for memory formation across the lifespan, facilitating the encoding, storage, and retrieval of information by modifying synaptic weights in response to experience. A key variant is spike-timing-dependent plasticity (STDP), which refines Hebbian learning by making synaptic changes dependent on the precise millisecond-scale timing of presynaptic and postsynaptic spikes. In STDP, as observed in cultured hippocampal neurons, if a presynaptic spike precedes a postsynaptic spike by 10-20 milliseconds, the synapse undergoes LTP, strengthening the connection; conversely, if the postsynaptic spike precedes the presynaptic one by a similar interval, LTD occurs, weakening it. This timing rule, with LTP windows up to 100 milliseconds and LTD up to 20 milliseconds in the reverse direction, allows for causal inference in neural signaling and supports sequence learning and predictive coding throughout development and adulthood.^[33]^[34]

Cortical Remapping

Cortical remapping, a form of functional neuroplasticity, involves the dynamic reorganization of sensory and motor maps within the cerebral cortex, leading to the expansion, contraction, or reassignment of representational areas such as somatotopic or retinotopic maps in response to altered sensory input or experience.^[35] This process allows the brain to adapt its cortical architecture to optimize processing efficiency, often building on underlying synaptic plasticity mechanisms.^[35] Several subtypes characterize cortical remapping. Homologous area adaptation occurs when a region in the undamaged hemisphere assumes responsibility for functions lost due to injury in the contralateral hemisphere, particularly evident in early development but possible in adults with targeted interventions.^[35] Cross-modal reassignment happens when a cortical area deprived of its primary sensory input begins processing information from an alternative modality; for instance, in congenitally blind individuals, the visual cortex activates during tactile tasks like Braille reading, as demonstrated by positron emission tomography studies showing significant occipital activation correlated with task performance. Compensatory masquerade refers to the repurposing of existing neural circuits to execute tasks through alternative behavioral strategies, without direct anatomical overlap, enabling functional recovery despite localized damage.^[35] Empirical evidence for cortical remapping comes from neuroimaging studies of skilled performers. In professional string musicians, magnetoencephalography revealed an enlarged cortical representation of the fingers of the left hand in the somatosensory cortex, with the extent of expansion correlating with the age at which training began and years of practice, indicating use-dependent plasticity.^[36] Functional magnetic resonance imaging has similarly shown map expansions in other domains, such as enlarged auditory cortical areas in musicians processing tonal sequences.^[35] Cortical remapping exhibits age-related limits, occurring more readily and extensively during developmental periods when the brain's plasticity is heightened due to ongoing circuit maturation, compared to adulthood where reorganization is constrained but can still be induced through intensive, repetitive training. In adults, such changes typically require prolonged exposure and may not fully restore pre-injury representations, highlighting the interplay between critical periods and lifelong adaptability.

Experience-Dependent Plasticity

Experience-dependent plasticity refers to the brain's ability to undergo adaptive structural and functional changes in response to specific environmental stimuli, sensory inputs, practice, or novel experiences, thereby refining neural circuits to better match ongoing demands and distinct from plasticity triggered by injury or deprivation.^[37] This form of plasticity enables the nervous system to continuously adjust to behavioral contexts, supporting learning and adaptation throughout life by strengthening or weakening synaptic connections based on relevance.^[38] Unlike innate developmental processes, it is highly influenced by the quality and timing of experiences, allowing for individualized neural reorganization.^[39] A prominent example of experience-dependent plasticity is the expansion of representational maps in the auditory cortex among musicians, where prolonged training leads to enlarged cortical areas dedicated to processing musical tones. In professional musicians, magnetoencephalography studies have shown significantly greater activation and spatial extent in the auditory cortex for piano tones compared to non-musicians, correlating with years of practice. Similarly, string players exhibit increased cortical representation of the digits of the left hand, demonstrating how repetitive sensory-motor practice can induce localized map expansions. These changes highlight how skill acquisition through dedicated practice drives targeted neural adaptations, enhancing perceptual acuity in relevant domains.^[40] At the mechanistic level, experience-dependent plasticity integrates long-term potentiation (LTP) and long-term depression (LTD) with behavioral reinforcement to stabilize synaptic modifications, where LTP strengthens active synapses during relevant experiences and LTD prunes less utilized ones.^[41] Attention plays a critical role in modulating these processes by gating synaptic changes, enhancing LTP induction in focused neural ensembles while suppressing irrelevant inputs through top-down influences on excitatory and inhibitory balance.00866-X) This integration ensures that plasticity is not random but tied to salient, rewarded behaviors, as seen in associative learning paradigms where dopamine signaling reinforces LTP-like changes.^[42] In development, sensitive periods amplify experience-dependent plasticity, particularly in early infancy, where exposure to specific stimuli shapes foundational neural wiring with heightened efficacy. For instance, during the first year of life, auditory exposure to native language phonemes refines phonetic discrimination circuits in the temporal lobe, establishing preferences that persist if not reinforced during this window.^[43] These periods are characterized by elevated expression of plasticity-related molecules, such as NMDA receptors, making the brain particularly responsive to environmental inputs that guide circuit maturation.^[44] Beyond infancy, such plasticity wanes but can be reactivated under intensive conditions, underscoring the lifelong yet developmentally peaked nature of experience-driven adaptations.^[45]

Clinical Applications

Recovery from Brain Injury and Stroke

Neuroplasticity plays a pivotal role in the rehabilitation of motor, cognitive, and sensory functions following traumatic brain injury or stroke by enabling the brain to reorganize neural circuits and compensate for damaged areas. This adaptive process allows surviving neurons to form new connections, strengthen existing ones, and recruit alternative pathways to restore lost functions, with recovery potential influenced by the extent of initial damage, timing of interventions, and individual factors such as age and lesion location.^[46] Key mechanisms include perilesional reorganization, where neural activity in the tissue surrounding the infarct zone increases to remap sensorimotor functions from damaged regions, supported by angiogenesis, neurogenesis, and reduced inhibitory signaling via GABA-A receptors. This process is enhanced by therapies that promote axonal remodeling and cell genesis in the ischemic penumbra, leading to improved tissue integrity and functional outcomes when initiated post-acutely. Complementing this, contralateral hemisphere recruitment involves activation of the unaffected hemisphere's motor areas, particularly in severe cases with large lesions, to compensate via uncrossed corticospinal tracts and homologous pathways, though excessive contralesional activity can sometimes impede full recovery by disrupting interhemispheric balance. Neuronal reorganization occurs in both ipsilesional and contralesional hemispheres, with early contralesional motor cortex involvement aiding initial motor recovery but shifting toward ipsilesional dominance for better long-term results.^[46]^[47] Therapies like constraint-induced movement therapy (CIMT) leverage use-dependent plasticity by restricting the unaffected limb to force intensive use of the impaired one, promoting motor relearning and cortical reorganization within the sensorimotor areas. Meta-analyses of randomized controlled trials demonstrate that modified CIMT yields small-to-medium effect sizes in improving upper limb motor function, arm-hand activities, and self-reported daily use, with sustained benefits up to four months post-intervention, particularly when applied within three months of stroke onset. These gains are linked to enhanced coordination and reduced reliance on compensatory strategies, fostering true neural repair through activity-driven synaptic strengthening.^[48] Longitudinal functional MRI studies provide evidence of these plastic changes correlating with recovery, such as in hand function, where sub-acute stroke patients show initial increased contralesional primary motor cortex activation during affected hand movements, which decreases post-therapy alongside improvements in clinical scores like the Fugl-Meyer Assessment. This shift indicates a progression from bilateral recruitment to more normalized ipsilesional patterns, with fractional anisotropy in the corticospinal tract predicting the extent of non-primary motor area involvement and functional gains after interventions like functional electrical stimulation.^[49] Recent advances as of 2025 include virtual reality (VR)-based therapies that enhance traditional rehabilitation by providing immersive environments to promote neuroplasticity, leading to improved motor outcomes in stroke recovery. AI-driven personalized protocols further optimize intervention timing and intensity based on individual plasticity profiles.^[50] Recovery unfolds across phases, beginning in the acute stage (first days to weeks) with resolution of diaschisis—a transient hypometabolism in remote brain regions like the contralateral cortex and subcortical structures—typically normalizing by day 8 in animal models and facilitating early spontaneous improvements in body function. The subacute phase (3 weeks to 6 months) features heightened plasticity, with significant gains in upper extremity function and activities of daily living, while the chronic phase (beyond 6 months, extending to years) allows continued, albeit modest, progress through targeted rehabilitation, challenging the notion of a fixed recovery plateau. A gradient of treatment sensitivity persists beyond one year, enabling ongoing neuroplastic adaptations even in late chronic stages.^[51]^[52]

Sensory Adaptation and Rehabilitation

Sensory adaptation in response to visual deprivation exemplifies cross-modal plasticity, where the visual cortex repurposes its functions to process tactile or auditory inputs. In blind individuals, functional magnetic resonance imaging (fMRI) studies have demonstrated that the primary visual cortex (V1) activates during Braille reading, a tactile task, indicating recruitment of visual areas for somatosensory processing.^[53] This activation occurs robustly in both early- and late-blind subjects, with early-blind individuals showing more extensive involvement of occipital regions, suggesting that the timing of sensory loss influences the degree of reorganization.^[54] Such adaptations enhance tactile discrimination, allowing proficient Braille readers to achieve speeds of approximately 100-200 words per minute, though generally slower than the 200-300 wpm visual reading speeds of sighted individuals.^[55] In the auditory domain, sensory loss due to deafness prompts similar plastic changes, particularly evident in rehabilitation via cochlear implants. These devices electrically stimulate the auditory nerve, triggering reorganization in the auditory cortex, where deprived regions regain responsiveness to sound within months post-implantation, as shown by electrophysiological recordings and imaging.^[56] For postlingually deaf adults, this reorganization correlates with improved speech perception, though excessive cross-modal invasion by visual inputs can sometimes hinder auditory recovery if implants are delayed.^[57] Human echolocation training further illustrates auditory plasticity; blind experts produce tongue clicks and interpret echoes to navigate space, with fMRI revealing activation in both auditory and visual cortices during echo processing, akin to visual spatial analysis in sighted individuals.^[58] Training-induced changes, observed after just weeks, include heightened sensitivity in primary auditory areas, underscoring the brain's capacity for rapid adaptation even in adulthood.^[59] Binocular vision development relies on neuroplastic mechanisms that align inputs from both eyes during critical periods, and disruptions like amblyopia—where one eye's input is suppressed—can be addressed through patching therapies that exploit residual plasticity. Patching the dominant eye forces use of the amblyopic eye, promoting cortical remapping and improvements in visual acuity and stereopsis, with gains up to two lines on acuity charts in children under 7 years.^[60] This treatment leverages homeostatic and Hebbian plasticity to restore binocular integration, as evidenced by reduced interocular suppression post-therapy in functional imaging studies.^[61] Even in older children and adults, combining patching with perceptual training extends the plastic window, yielding durable binocular vision enhancements.^[62] Positron emission tomography (PET) scans provide direct evidence of auditory cortex adaptations in deaf signers, revealing expanded activation in superior temporal regions during sign language processing, which overlaps with areas typically dedicated to spoken language in hearing individuals.^[63] This reorganization, observed in congenitally deaf users of American Sign Language, includes bilateral engagement of auditory association areas for linguistic features like motion and spatial syntax, compensating for auditory deprivation through visual-linguistic plasticity.^[64] Such findings highlight how sensory loss drives cortical expansion and functional repurposing, informing rehabilitation strategies that preserve native sensory maps where possible.

Management of Chronic Pain and Phantom Limbs

Neuroplasticity plays a critical role in the development of phantom limb pain (PLP) following amputation, where maladaptive cortical remapping occurs in the primary somatosensory cortex (S1). After limb loss, the deafferented cortical area representing the missing limb is invaded by adjacent representations, such as those for the face or upper arm, leading to referred sensations and pain when stimuli are applied to these neighboring body parts. This reorganization is evidenced by magnetoencephalography and functional imaging studies showing expanded representations of adjacent areas encroaching on the former limb territory, correlating with PLP intensity.^[65]^[66] Therapeutic interventions leverage neuroplasticity to reverse this maladaptive remapping and alleviate PLP. Mirror box therapy, pioneered by V.S. Ramachandran in the 1990s, uses a mirror to create a visual illusion of the intact limb, enabling patients to perform movements that activate the motor and sensory cortices as if the phantom limb were present, thereby reducing pain through restored cortical representation. Clinical trials have demonstrated significant PLP relief in a substantial proportion of patients after regular use, with effects persisting for months.^[67]^[68] Graded motor imagery (GMI), developed by G. Lorimer Moseley, involves a sequential progression from implicit motor imagery (recognizing limb laterality), to explicit motor imagery (visualizing movements), and finally to mirror therapy, progressively reactivating the motor cortex to normalize somatotopic maps and decrease pain. Randomized controlled trials of GMI in amputees have shown reductions in PLP by 30-50% compared to controls, attributed to enhanced neuroplastic changes in the premotor and primary motor cortices.^[69] Recent developments as of 2025 incorporate virtual reality (VR) versions of mirror therapy, providing immersive, customizable illusions to enhance cortical remapping and pain relief in PLP. Noninvasive brain stimulation techniques, such as transcranial magnetic stimulation, further modulate maladaptive plasticity for chronic pain management.^[50]^[70] In broader chronic pain conditions, neuroplasticity contributes to central sensitization, where amplified synaptic plasticity in spinal and supraspinal pain pathways heightens nociceptive signaling. This involves long-term potentiation (LTP)-like mechanisms at synapses in the dorsal horn and thalamus, lowering pain thresholds and expanding receptive fields, as seen in conditions like fibromyalgia and neuropathic pain. Interventions targeting this plasticity, such as cognitive-behavioral therapies or neuromodulation, can reverse sensitization by promoting synaptic depression and restoring balanced neural activity. Functional MRI (fMRI) studies of PLP therapies illustrate this reversibility: after mirror therapy or GMI, there is normalization of S1 maps, with reduced overlap from adjacent areas and decreased activation during phantom sensations, correlating with pain reduction.^[66]^[71]

Developmental and Learning Applications

Early Child Development

Neuroplasticity plays a pivotal role in early child development, particularly during critical and sensitive periods when the brain exhibits heightened adaptability to environmental inputs, shaping sensory, linguistic, and social capabilities.^[43] These periods represent windows of elevated plasticity, typically from birth to around seven years, during which experiences profoundly influence neural circuit formation. For vision, the most sensitive period within the first two to three years allows rapid refinement, but the overall critical period extends up to around 7-8 years, during which sensory deprivation or imbalance can lead to lasting deficits like amblyopia if not addressed timely.^[72] In language development, a sensitive period for phoneme discrimination emerges between six and twelve months, where infants attune to native speech sounds through perceptual narrowing, losing sensitivity to non-native contrasts by age seven without exposure; this process relies on experience-dependent mechanisms in the auditory cortex to strengthen relevant neural representations.^[43] Similarly, attachment formation occurs during a sensitive period in early infancy, extending through the first two years, enabling the brain to form enduring social bonds via specialized circuitry in regions like the amygdala and prefrontal cortex, which supports adaptive behaviors essential for survival and emotional regulation.^[73] Enriched environments, characterized by diverse sensory, social, and cognitive stimuli, accelerate myelination and modulate synapse pruning, thereby enhancing brain maturation in young children. Studies in animal models, applicable to human development, demonstrate that prolonged environmental enrichment from postnatal weeks two to twelve increases oligodendrocyte maturation and myelin thickness in white matter tracts, improving neural efficiency and motor coordination without altering axon numbers initially.^[74] In children, such environments delay synaptic pruning in prefrontal areas, preserving network complexity and extending plasticity into later childhood, as evidenced by thicker cortices in higher socioeconomic settings with greater cognitive stimulation.^[75] This modulation follows Hebbian principles, where correlated neural activity from enriched experiences strengthens synapses and promotes adaptive rewiring, contrasting with deprivation that hastens pruning and limits developmental potential.^[75] In neurodevelopmental disorders like attention-deficit/hyperactivity disorder (ADHD), neuroplasticity in executive function networks is often impaired, affecting inhibitory control and working memory in school-aged children. ADHD-related deficits arise from atypical synaptic pruning and myelination in frontal-striatal circuits, leading to reduced adaptability in prefrontal regions responsible for attention and decision-making.^[76] Behavioral therapies, such as cognitive-behavioral interventions, leverage remaining plasticity to improve these functions by targeting skill-based training that rewires neural pathways, with meta-analyses showing moderate gains in executive performance comparable to pharmacological effects.^[77] These interventions are most effective when initiated early, capitalizing on the brain's heightened malleability to mitigate long-term cognitive impairments.^[78] Longitudinal studies underscore the role of secure attachment in fostering social brain development through neuroplastic changes. The Bucharest Early Intervention Project followed institutionalized Romanian children and found that foster care placement before fifteen months reduced amygdala hyperactivity and cognitive deficits compared to later interventions, promoting normalized social-emotional trajectories via enhanced prefrontal-amygdala connectivity.^[79] Similarly, research tracking mother-child dyads from infancy to age ten revealed that consistent caregiving correlates with refined insula and anterior cingulate responses to social cues, supporting empathy and attachment security as the brain prunes irrelevant connections and strengthens relational networks.^[79] These findings highlight how early social experiences drive lasting plasticity in the social brain, with disruptions like maternal depression accelerating maladaptive changes in limbic structures.^[79]

Language Acquisition and Multilingualism

Neuroplasticity plays a pivotal role in language acquisition by enabling the brain to adapt and reorganize neural circuits in response to linguistic input throughout the lifespan. During early childhood, heightened plasticity facilitates the rapid integration of phonological, syntactic, and semantic structures, allowing children to achieve native-like proficiency in their first language. This process involves dynamic changes in synaptic connections and cortical mapping, particularly in perisylvian regions of the left hemisphere, where exposure to language stimuli strengthens relevant pathways. As individuals encounter additional languages, neuroplastic mechanisms support the formation of overlapping yet distinct neural representations, enhancing overall linguistic flexibility.^[80] In bilingual and multilingual individuals, sustained language use induces structural and functional neuroplasticity, notably increasing gray matter density in key language areas such as the inferior frontal gyrus and superior temporal gyrus. These changes reflect experience-dependent remodeling, where frequent switching between languages promotes denser connectivity in white matter tracts like the arcuate fasciculus, supporting efficient processing of multiple linguistic systems. Additionally, bilingualism enhances executive control functions through prefrontal cortex plasticity, improving cognitive flexibility, attention, and inhibition as the brain adapts to manage interference between languages. For instance, lifelong bilinguals exhibit greater prefrontal activation during task-switching paradigms, demonstrating how neuroplasticity bolsters cognitive efficiency.^[81]^[82]^[83]^[84] The concept of critical periods underscores the age-dependent nature of neuroplasticity in language learning, with optimal acquisition of native-like accents and grammar typically occurring before puberty due to peak synaptic pruning and myelination. Evidence from longitudinal studies indicates that second language learners who begin before age 10-12 achieve higher proficiency in subtle phonetic distinctions, as early plasticity allows for more precise tuning of auditory and motor cortices. In contrast, adults face challenges from reduced plasticity, often relying on compensatory strategies like leveraging declarative memory networks in the hippocampus and right hemisphere, though they can still attain functional fluency through intensive practice. This shift highlights how neuroplasticity diminishes but persists, enabling adaptations such as increased reliance on semantic processing over rote memorization.^[85]^[86] Functional magnetic resonance imaging (fMRI) studies reveal plasticity in hemispheric dominance among multilinguals, with early bilinguals showing robust left-hemisphere lateralization for language tasks, while late learners exhibit more bilateral activation as the brain recruits additional networks for compensation. In multilingual speakers, fMRI data demonstrate dynamic shifts, such as reduced left-hemisphere exclusivity during code-switching, reflecting adaptive reorganization that enhances cognitive reserve. These findings illustrate how neuroplasticity allows the multilingual brain to redistribute workload across hemispheres, optimizing performance in complex linguistic environments.^[87]^[88] Multilingualism fosters long-term neuroplasticity that contributes to cognitive reserve, delaying the onset of dementia symptoms by approximately four to five years compared to monolinguals. This protective effect arises from sustained bilingual engagement, which maintains neural efficiency and promotes compensatory recruitment of alternative pathways in the face of age-related degeneration. Studies of Alzheimer's patients show that multilingual individuals exhibit denser gray matter in frontal and temporal regions at diagnosis, attributing this resilience to lifelong plasticity that buffers against pathological changes. Such benefits extend across the lifespan, as ongoing language use reinforces synaptic integrity and executive functions, underscoring multilingualism's role in preserving cognitive health.^[89]^[90]^[91]

Skill Acquisition in Adulthood

In adulthood, neuroplasticity enables the acquisition of new skills through mechanisms such as deliberate practice, which promotes structural and functional reorganization in the brain, including the expansion of cortical maps associated with specific tasks. This process builds on foundational synaptic plasticity, where repeated activation strengthens neural connections to support learning. For instance, intensive training can lead to measurable changes in brain regions involved in motor and cognitive functions, allowing adults to develop expertise in areas like navigation or manual dexterity.^[92] A seminal example is the structural adaptation observed in London taxi drivers, who undergo rigorous training to memorize complex city routes. In a study of 16 licensed taxi drivers compared to 50 controls, magnetic resonance imaging revealed significantly larger posterior hippocampal volumes in drivers, correlating positively with years of experience (r=0.6, P<0.05), while anterior hippocampal volumes were smaller. These findings indicate experience-dependent plasticity, where navigational demands induce hippocampal expansion to enhance spatial memory and route-finding efficiency.^[93] Although neuroplasticity in adults proceeds more slowly than in youth due to reduced synaptic flexibility and neurogenesis rates, it remains robust and can be facilitated by techniques like spaced repetition and high motivation. Spaced repetition, involving distributed practice sessions, enhances long-term retention by promoting hippocampal neurogenesis and strengthening memory traces, as evidenced by improved episodic memory performance in adults through increased neural pattern reinstatement during retrieval. Motivation further amplifies these effects by increasing dopamine release, which supports synaptic consolidation during skill practice.^[94]^[95] These principles underpin applications in vocational training and expertise development, where targeted interventions leverage plasticity to build professional competencies. Reviews of training-induced learning show that adults engaging in progressive motor or cognitive exercises exhibit cortical reorganization, leading to skill mastery in fields like surgery or instrumentation, with functional improvements sustained over months of deliberate practice. Such approaches emphasize individualized progression to overcome age-related barriers, fostering lifelong adaptability in the workforce.^[96]^[97]

Lifestyle and Environmental Influences

Physical Exercise and Fitness

Physical exercise, particularly aerobic and resistance training, promotes neuroplasticity by inducing physiological changes that enhance brain structure and function. These changes occur through the upregulation of growth factors that support neuronal survival, differentiation, and synaptic remodeling.^[98]^[99] A key mechanism involves increased expression of brain-derived neurotrophic factor (BDNF), which is elevated in response to exercise-induced signaling pathways, leading to enhanced hippocampal neurogenesis. In rodent models, voluntary wheel-running has been shown to boost BDNF levels and proliferation of new neurons in the hippocampus, effects that translate to humans through improved synaptic plasticity and cognitive outcomes. Aerobic exercises, such as running, primarily target the hippocampus, promoting volume increases and neurogenesis that support memory consolidation, while resistance training influences frontal brain regions, enhancing executive function and neural efficiency.^[99]^[98]^[100]^[101] These neuroplastic adaptations yield benefits like improved memory and mood regulation, as exercise strengthens synaptic connections and reduces inflammation in brain tissue. Meta-analyses indicate that regular physical activity delays cognitive decline in older adults, with aerobic interventions increasing hippocampal volume by 1-2% and leading to modest improvements in executive function, while combined aerobic and resistance programs show greater protective effects against age-related neurodegeneration.^[102]^[103]

Meditation and Mindfulness Practices

Meditation and mindfulness practices induce neuroplasticity by reshaping neural circuits involved in attention, emotion regulation, and stress responses, fostering adaptive changes through repeated focused awareness and non-judgmental observation. These practices leverage experience-dependent plasticity to alter brain structure and function, enhancing resilience to psychological stressors and improving cognitive control. Longitudinal neuroimaging studies have consistently demonstrated these effects, highlighting meditation's role in preventive mental health maintenance. In long-term meditators, structural changes include cortical thickening in the prefrontal cortex, which supports executive functions like decision-making and attention, and the insula, which aids in interoceptive awareness and emotional processing.^[104] Additionally, these practitioners show reduced amygdala reactivity to emotional stimuli, correlating with lowered stress and anxiety responses by dampening the brain's fear circuitry.^[105] Such alterations underscore meditation's capacity to recalibrate limbic-prefrontal interactions for better emotion regulation. Mindfulness-Based Stress Reduction (MBSR) programs, an 8-week structured intervention involving daily meditation and yoga, have been linked to measurable structural brain changes, including increased gray matter density in the hippocampus (involved in memory and stress regulation) and posterior cingulate cortex (key for self-referential processing).^[106] Foundational evidence from cross-sectional MRI studies, such as those by Lazar et al. (2005), established patterns of cortical thickening in experienced meditators, while longitudinal research like Hölzel et al. (2011) extended these findings to shorter interventions and specific regions like the hippocampus.^[104]^[106] Recent advancements, including psilocybin-assisted mindfulness training, reveal enhanced neuroplastic effects, such as sustained modulation of the default mode network (DMN)—a system associated with mind-wandering and self-referential thought—with reduced connectivity persisting months post-intervention.^[107] These changes are driven by mechanisms like DMN downregulation through attentional plasticity, where sustained focus during meditation strengthens task-positive networks while suppressing rumination-prone activity.^[108] This targeted reconfiguration promotes clearer cognition and emotional stability, distinguishing contemplative practices as potent tools for neural adaptation.

Environmental Enrichment

Environmental influences, such as exposure to enriched settings with novel stimuli, social interactions, and cognitive challenges, significantly enhance neuroplasticity by promoting structural and functional brain changes. In animal models, enriched environments increase dendritic branching, synaptic density, and neurogenesis in regions like the hippocampus, mediated by elevated BDNF levels and reduced stress hormones. These effects translate to humans through lifestyle elements like varied daily routines or urban green spaces, which correlate with better cognitive reserve and delayed neurodegeneration. Human studies, including cohort analyses, show that greater environmental complexity in early life and adulthood supports synaptic remodeling and improves learning outcomes, though long-term impacts require further research as of 2025.^[1]^[2]

Artistic and Musical Engagement

Engagement in musical activities has been shown to induce significant neuroplastic changes in the brain, particularly among professional musicians. Structural neuroimaging studies reveal an enlarged corpus callosum in musicians compared to non-musicians, facilitating enhanced interhemispheric communication essential for coordinating bimanual motor skills during performance.^[109] This enlargement is more pronounced in those who begin training early in life, suggesting that prolonged practice drives white-matter plasticity in this region.^[110] Additionally, musicians exhibit greater gray-matter volume in Heschl's gyrus, the primary auditory cortex, which correlates with heightened activation and sensitivity to musical stimuli, reflecting experience-dependent reorganization of auditory processing areas.^[111] Musical practice further promotes auditory-motor integration, a key aspect of sensory-motor plasticity. Through repetitive training, musicians develop stronger functional connectivity between auditory and motor cortices, enabling precise synchronization of sound perception with physical execution, such as in piano playing.^[112] This integration is evident even after short-term practice sessions, where neural co-activation in these regions strengthens, supporting the brain's ability to adapt motor responses to auditory cues. Such changes underscore music's role in fostering coordinated neural networks for complex, real-time sensory-motor tasks. In artistic pursuits, particularly art therapy, creative expression enhances emotional processing via plasticity in the visual cortex. Art-making activities engage visual areas to externalize and reprocess trauma-related imagery, promoting adaptive rewiring that reduces hyperarousal and improves emotional regulation in individuals with post-traumatic stress disorder (PTSD).^[113] Randomized controlled trials demonstrate that trauma-focused art therapy significantly alleviates PTSD symptoms, including intrusive memories and avoidance, by facilitating the integration of fragmented sensory experiences through visual representation.^[114] This approach leverages the visual cortex's adaptability to transform distressing visual encodings of trauma into coherent narratives, aiding recovery. These creative engagements drive neuroplasticity through mechanisms of multisensory integration, which foster cross-modal plasticity across sensory domains. In music, the coupling of auditory, motor, and tactile inputs during performance strengthens multimodal neural pathways, enhancing overall perceptual acuity.^[115] Similarly, in art therapy, drawing tasks promote cross-modal memory plasticity by recruiting visual cortex resources to bolster verbal and emotional recall, as seen in improved memory performance following brief training.^[116] This integration not only supports sensory-motor refinement but also emotional resilience by enabling the brain to reconfigure connections between disparate modalities.

Emerging and Advanced Topics

Neuroplasticity in Aging and Neurodegeneration

As individuals age, neuroplasticity undergoes significant changes, characterized by a decline in key molecular and structural mechanisms that support synaptic adaptability. Brain-derived neurotrophic factor (BDNF), a critical protein for promoting neuronal survival and synaptic plasticity, shows reduced expression and plasma levels with advancing age, correlating with diminished cognitive performance across decades of life.^[117] Similarly, synaptic density decreases, accompanied by impaired long-term potentiation (LTP) and long-term depression (LTD), which are essential for learning and memory formation.^[2] In healthy aging, however, the brain can exhibit compensatory recruitment, where remaining neural networks adapt to offset losses through enhanced functional connectivity and recruitment of alternative pathways, helping to maintain cognitive stability despite these declines.^[118] In neurodegenerative diseases, these age-related alterations are exacerbated, disrupting plasticity and accelerating cognitive and motor deficits. In Alzheimer's disease, amyloid-beta (Aβ) oligomers impair synaptic plasticity by inhibiting LTP and promoting excessive LTD, leading to synaptic dysfunction and memory loss even before widespread neuronal death.^[119] This Aβ-mediated interference overrides normal activity-dependent synaptic mechanisms, contributing to the progression of cognitive decline.^[120] In Parkinson's disease, neuroplasticity manifests through adaptive changes in motor circuits, where compensatory mechanisms in cortical and subcortical networks attempt to mitigate dopamine loss; for instance, enhanced corticospinal excitability and network reorganization can temporarily sustain motor function amid neurodegeneration.^[121] These adaptations highlight plasticity's role in disease progression, though they often become insufficient as pathology advances.^[122] Interventions targeting neuroplasticity offer promise for preserving function in aging and neurodegeneration. Cognitive training programs induce neural plastic changes, enhancing synaptic efficiency and behavioral outcomes in older adults by counteracting age-related declines.^[123] The Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study, a landmark randomized controlled trial initiated in 2002 and followed longitudinally, demonstrated that targeted cognitive interventions—such as memory, reasoning, and speed-of-processing training—improve cognitive abilities and delay functional decline in daily living for up to 10 years post-training.^[124] These effects are attributed to training-induced plasticity, including increased prefrontal and hippocampal activation. Recent advancements as of 2025 include gene therapy trials aimed at enhancing neuroplasticity in dementia. A first-in-human clinical trial at the University of California San Diego is testing continuous brain delivery of BDNF via gene therapy to protect neurons and restore synaptic plasticity in early Alzheimer's patients, with preliminary data suggesting potential preservation of cognitive function by bolstering neurotrophic support.^[125] Such approaches build on evidence that elevating BDNF levels can counteract amyloid-induced plasticity deficits, offering a targeted strategy to mitigate neurodegeneration.^[126]

Animal Models and Comparative Studies

Animal models have been instrumental in elucidating the mechanisms of neuroplasticity, particularly through controlled experiments that isolate environmental and injury-related influences on brain structure and function. In rodents, such as mice and rats, environmental enrichment—characterized by complex housing with toys, social interaction, and novel stimuli—significantly enhances hippocampal neurogenesis, the birth and integration of new neurons in the dentate gyrus. A seminal study demonstrated that adult mice in enriched environments exhibit approximately twice as many new neurons in the hippocampus compared to those in standard cages, with these neurons surviving and integrating into functional circuits to support learning and memory.^[127] This plasticity is activity-dependent, as voluntary exercise and cognitive challenges further promote the proliferation and differentiation of neural precursors in the subgranular zone.^[128] Rodent models also reveal neuroplasticity in response to traumatic brain injury (TBI), where compensatory mechanisms mirror aspects of recovery observed in other contexts. In controlled cortical impact models of TBI in mice, injury induces a shift in neural stem cell fate toward increased neurogenesis at the expense of astrogliogenesis, leading to partial functional recovery through circuit reorganization.^[129] Similarly, blockade of the CCR5 chemokine receptor enhances recovery in mouse models of stroke and traumatic brain injury (TBI) by promoting synaptic plasticity, including dendritic spine formation, highlighting molecular targets for intervention.^[130] These findings underscore how injury triggers adaptive remodeling, including axonal sprouting and synaptogenesis, to restore behavioral outputs like locomotion. Comparative studies across species illuminate evolutionary variations in neuroplasticity, with notable differences between rodents and primates in cortical wiring. Primate cortical neurons, unlike their rodent counterparts, form sparser excitatory and inhibitory connections—receiving 2–5 times fewer synapses per neuron—potentially enabling more flexible plasticity in higher-order processing areas.^[131] In songbirds, such as zebra finches and canaries, the song control system exemplifies vocal learning plasticity, where nuclei like HVC and RA undergo seasonal volumetric changes driven by hormonal cues, allowing adult birds to refine or expand their repertoire.^[132] Food-storing birds, like black-capped chickadees, display complementary hippocampal plasticity, with volume and neurogenesis peaking in autumn to support spatial memory for cache sites, demonstrating experience-dependent structural adaptations. Post-2010 advances in optogenetics have provided causal insights into plasticity circuits in these models. By selectively activating or silencing genetically targeted neurons with light, studies in rodents have shown that optogenetic stimulation of corticospinal pathways post-spinal injury reroutes signals through alternative circuits, restoring motor function via enhanced synaptic strengthening.^[133] In songbirds, optogenetic manipulation of auditory-vocal circuits reveals how precise temporal patterns drive long-term potentiation-like changes, essential for sequence learning. These techniques highlight conserved yet species-specific mechanisms, with implications for understanding human brain adaptability.

Enhancement in Transhumanism and Brain-Computer Interfaces

In transhumanism, brain-computer interfaces (BCIs) represent a pivotal technology for transcending biological limitations, enabling cognitive and sensory enhancements that integrate human neural processes with artificial systems. Proponents view BCIs as tools to augment intelligence, extend sensory perception, and achieve seamless human-machine symbiosis, drawing on the brain's inherent neuroplasticity to facilitate adaptation and long-term integration. This perspective aligns with transhumanist goals of radical life extension and capability enhancement, as articulated in foundational definitions emphasizing applied science to evolve beyond human constraints.^[134] Neuroplasticity serves as the biological foundation for BCI efficacy in enhancement contexts, allowing the brain to reorganize neural pathways in response to interface-mediated feedback. Through mechanisms like Hebbian plasticity—where coincident neural activation strengthens synaptic connections—BCIs provide real-time neurofeedback that reinforces targeted brain activity, leading to lasting cortical reorganization. For instance, closed-loop BCIs decode neural signals for device control while delivering sensory inputs, such as haptic feedback, which the brain incorporates into its body schema over days to weeks of use. This plasticity-driven adaptation has been demonstrated in non-human primates, where subjects learned to control robotic arms via cortical implants, effectively extending their motor capabilities through neural remapping.^[135]^[136] In human applications, BCIs leverage neuroplasticity to restore and potentially surpass natural functions, aligning with transhumanist visions of selective perfectibility. Early experiments at Duke University in the 1990s showed paralyzed individuals modulating neural activity to operate cursors or prosthetics, with plasticity enabling improved control accuracy through operant conditioning of motor cortex neurons. More advanced bidirectional BCIs, incorporating both motor output and artificial sensory input, have enabled tetraplegic patients to perceive touch via intracortical stimulation, fostering rapid integration where the brain treats prosthetic sensations as native. These developments suggest transhumanist potential for cognitive enhancements, such as accelerated learning or direct knowledge upload, though current implementations prioritize therapeutic restoration over augmentation.^[134]^[137] Challenges in this domain include optimizing BCI parameters to maximize plasticity without overload, as delays exceeding 200-300 ms or mismatched feedback modalities can hinder adaptation. Transhumanist advocates, however, emphasize ethical imperatives for equitable access to prevent exacerbating social inequalities, echoing Julian Huxley's original call for inclusive enhancement. Ongoing research, such as Neuralink's implantable devices, continues to explore how induced plasticity could enable broader enhancements like multilingual fluency or enhanced memory, though long-term human data remains limited.^[135]^[134]

Limitations and Future Directions

Maladaptive Plasticity

Maladaptive neuroplasticity refers to the brain's ability to reorganize in ways that contribute to pathological conditions rather than adaptive recovery, often exacerbating symptoms in neurological and psychiatric disorders.^[138] This process can lead to dysfunctional neural circuits that perpetuate maladaptive behaviors or sensations, highlighting the double-edged nature of plasticity where experience-dependent changes become counterproductive.^[139] A prominent example is tinnitus, where hearing loss triggers hyperactivity and reorganization in the central auditory pathways, resulting in the perception of phantom sounds due to maladaptive strengthening of neural maps.^[140] In this condition, reduced input from peripheral damage leads to increased spontaneous firing and synchrony among auditory neurons, expanding the representation of the affected frequency range in a way that generates persistent auditory hallucinations.^[139] Similarly, in addiction, repeated drug exposure strengthens reward circuits through maladaptive plasticity, particularly in the mesolimbic dopamine pathway, where cues associated with substances hijack normal reinforcement mechanisms to drive compulsive seeking.^[141] This reinforcement creates a persistent memory trace that overrides natural rewards, contributing to relapse even after prolonged abstinence.^[142] Key mechanisms underlying these maladaptations include aberrant long-term potentiation (LTP) in pain and anxiety pathways, which amplifies synaptic efficacy beyond normal levels and sustains hypersensitivity.^[143] In chronic pain states, for instance, this leads to central sensitization where innocuous stimuli evoke exaggerated responses due to enhanced excitatory transmission.^[144] Additionally, loss of inhibitory control, often involving reduced GABAergic modulation, allows unchecked excitation that further entrenches dysfunctional circuits, as seen in various sensory and emotional disorders.^[138] Functional magnetic resonance imaging (fMRI) studies in post-traumatic stress disorder (PTSD) provide compelling evidence of hyperplastic fear responses, revealing heightened amygdala activation and altered connectivity in fear-processing networks that fail to extinguish after trauma.^[145] These changes reflect maladaptive plasticity where fear memories become overly consolidated, leading to persistent hyperarousal and avoidance behaviors.^[146] Interventions targeting maladaptive plasticity, such as extinction training, aim to reverse these changes by promoting new learning that weakens pathological associations, as demonstrated in exposure therapies modeled on fear extinction paradigms.^[147] In PTSD models, this approach restores inhibitory control over fear circuits, reducing symptom severity through targeted synaptic remodeling.^[148] Clinical applications in pain management similarly leverage plasticity-reversing techniques to mitigate central sensitization.^[144]

Critical Periods and Constraints

Critical periods represent discrete temporal windows during development when the brain exhibits heightened sensitivity to environmental stimuli, allowing for profound structural and functional changes that shape neural circuits. These periods are essential for establishing sensory, motor, and cognitive abilities, such as visual acuity and language acquisition. In the visual system, for instance, the critical period in kittens spans from eye opening to approximately three months of age, during which monocular deprivation leads to permanent shifts in ocular dominance columns in the visual cortex. In humans, analogous windows extend over years, with early childhood being pivotal for binocular vision development; deprivation beyond this period results in enduring deficits like amblyopia. The onset and closure of these periods are tightly regulated by molecular mechanisms, including the maturation of inhibitory neurotransmission via GABAergic circuits involving parvalbumin-positive interneurons, which stabilize neural networks and limit further plasticity.^[149] Several factors impose constraints on neuroplasticity within and beyond these critical periods, modulating the brain's capacity for adaptation. Hormonal influences, particularly gonadal steroids like estrogen and testosterone, play a key role in timing and intensity of plasticity; for example, surges during puberty can either enhance synaptic remodeling in cortical areas or constrain it by promoting circuit stabilization. Sleep deprivation disrupts this process by impairing synaptic consolidation and reducing dendritic spine density in regions like the hippocampus and visual cortex, thereby diminishing experience-dependent plasticity during sensitive developmental windows.^[150] Genetic factors further delimit plasticity; mutations in the FOXP2 gene, a transcription factor critical for neural development, impair synaptic plasticity and neurite outgrowth in language-related brain areas, leading to deficits in speech acquisition if occurring during the relevant critical period for vocal learning. These constraints ensure that plasticity is not indefinite, preventing maladaptive changes while allowing targeted refinement of neural functions. Efforts to reopen closed critical periods have shown promise through pharmacological interventions that target inhibitory mechanisms. In animal models, valproate, a histone deacetylase inhibitor, restores juvenile-like plasticity in the adult visual cortex by reducing GABAergic inhibition, enabling recovery from monocular deprivation-induced amblyopia when combined with visual training. Similar approaches have extended to auditory domains, where valproate administration in adult humans improved absolute pitch learning, a skill typically confined to early childhood critical periods. These findings highlight the potential for transiently lifting natural constraints to harness neuroplasticity for therapeutic purposes, though long-term effects and specificity require further investigation.^[151]

Recent Advances and Research Gaps

Recent research has demonstrated that psilocybin, a psychedelic compound, promotes structural neuroplasticity by inducing rapid and persistent growth of dendritic spines in the prefrontal cortex, offering potential therapeutic benefits for depression. In preclinical models, a single dose of psilocybin increases spine density and size by approximately 10% within 24 hours, an effect mediated by 5-HT2A receptor activation and downstream pathways involving BDNF/TrkB signaling and mTORC1, with changes lasting up to a month. These adaptations reverse synaptic deficits associated with chronic stress and major depressive disorder, contributing to sustained antidepressant effects observed in clinical trials for treatment-resistant depression.^[152]^[153]^[154] Advancements in AI-driven neurofeedback have enabled personalized training protocols to enhance neuroplasticity, particularly in cognitive rehabilitation. These systems use machine learning algorithms to analyze real-time brain activity from EEG or fMRI data, adapting feedback to individual neural patterns and optimizing synaptic strengthening for targeted outcomes like attention or memory improvement. For instance, AI reduces latency in neurofeedback loops by up to 50-fold, allowing precise modulation of brain states to promote plasticity in conditions such as traumatic brain injury.^[155]^[156] Emerging technologies like optogenetics delivered via viral vectors are advancing precise control of neural circuits in human tissue, with implications for modulating plasticity. Adeno-associated virus serotype 9 (AAV9) has been used to transduce human hippocampal slices from epilepsy patients, expressing light-sensitive channelrhodopsins in excitatory neurons to inhibit hyperexcitable activity and potentially restore balanced plasticity. This approach achieves network-level suppression of firing rates by over 90% in responsive neurons, paving the way for therapeutic applications in cognitive disorders.^[157]^[158] Epigenome editing tools are being developed to sustain neuroplasticity by targeting gene expression in specific neuronal populations. These methods offer promise for long-term reversal of plasticity deficits in aging or neurological conditions. In the context of 2025, post-COVID research has intensified focus on long-haul cognitive effects, revealing persistent deficits in executive function, memory, and processing speed that may involve disrupted neuroplasticity. Studies using FDG-PET imaging have shown hypometabolism in frontal and temporal regions in post-COVID patients with cognitive decline, assessed at around 5 months post-infection. Additionally, as of 2024, up to 60% of long COVID patients report persistent neurological symptoms, including brain fog, up to three years post-infection, underscoring the need for plasticity-targeted interventions like neuromodulation to mitigate these structural and functional alterations.^[159]^[160]^[161] Despite these advances, significant research gaps remain, including understudied sex differences in neuroplasticity. Females demonstrate greater white matter changes, such as increased fractional anisotropy in tracts like the corticospinal tract following motor training, yet most studies aggregate data across sexes, overlooking these disparities due to historical biases and limited funding for sex-specific analyses.^[162]^[163] The long-term effects of digital media on adolescent brain plasticity are also poorly understood, with cross-sectional data suggesting associations between high screen time and altered cortical thickness or connectivity, but lacking longitudinal neuroimaging to clarify causal mechanisms or interactions with factors like socioeconomic status.^[164]^[165] Furthermore, integrating quantum computing models for simulating neuroplasticity remains a nascent gap, as classical computers struggle with the combinatorial complexity of synaptic dynamics in large-scale neural networks, while quantum algorithms like Grover's show potential for inferring activity patterns but require further development for plasticity-specific time evolution.

References

[1]
Neuroplasticity - StatPearls - NCBI Bookshelf - NIH
It is defined as the ability of the nervous system to change its activity in response to intrinsic or extrinsic stimuli by reorganizing its structure, functions ...Continuing Education Activity · Introduction · Issues of Concern
[2]
Exploring the Role of Neuroplasticity in Development, Aging, and ...
Neuroplasticity refers to the ability of the brain to reorganize and modify its neural connections in response to environmental stimuli, experience, learning, ...
[3]
Hippocrates: a pioneer in the treatment of head injuries - PubMed
Hippocrates' treatise On Wounds in the Head represents an excellent source of information regarding the extent of experience with head injuries in classical ...
[4]
Marie-Jean-Pierre Flourens (1794–1867) and Cortical Localization
Mar 17, 2009 · Flourens did not favour the idea of cerebral localization and concluded that the brain functioned as a whole and thus arose the concept of 'cerebral ...
[5]
Neuronal plasticity: historical roots and evolution of meaning - PubMed
In this paper, we outline some important milestones in the history of the term "plasticity" in reference to the nervous system.
[6]
The Legacy of the Kennard Principle - PMC - NIH
In 1936, Margaret Kennard introduced the concept of brain plasticity in an animal model by studying the recovery of motor functions after performing brain ...
[7]
MODALITY AND TOPOGRAPHIC PROPERTIES OF SINGLE ...
MODALITY AND TOPOGRAPHIC PROPERTIES OF SINGLE NEURONS OF CAT'S SOMATIC SENSORY CORTEX. Vernon B. Mountcastle. Vernon B. Mountcastle.Missing: revival | Show results with:revival
[8]
Still searching for the engram - PMC - PubMed Central - NIH
Lashley's systematic work was guided by the then prevalent and straightforward view that stimulus-response learning is supported by connections between sensory ...
[9]
Fifty Years Since Lashley's In Search of the Engram: Refutations and ...
Aug 7, 2025 · Lashley's research was an attempt to find the location in the brain responsible for learning and memory traces, a hypothetical structure he ...Missing: fixed | Show results with:fixed
[10]
The Search for the Engram, II - SpringerLink
Lashley, K.S. In search of the engram. In Symposium of the society for experimental biology (Vol. 4). New York: Cambridge University Press, 1950. Google Scholar.
[11]
[PDF] David H. Hubel - Nobel Lecture
It led to a study of the pre- and postnatal visual development of ocular dominance columns, and the effects of visual deprivation on the columns, which Torsten ...
[12]
Somatosensory cortical map changes following digit amputation in ...
Apr 20, 1984 · The cortical representations of the hand in area 3b in adult owl monkeys were defined with use of microelectrode mapping techniques 2-8 months after surgical ...
[13]
Somatosensory cortical map changes following digit amputation in ...
Apr 20, 1984 · Somatosensory cortical map changes following digit amputation in adult monkeys. Dr. Michael M. Merzenich,.
[14]
Tactile sensory substitution studies - PubMed
A project to explore late brain plasticity was initiated that was to lead into a broad area of sensory substitution studies.
[15]
Vision Substitution by Tactile Image Projection - Nature
Published: 08 March 1969. Vision Substitution by Tactile Image Projection. PAUL BACH-Y-RITA,; CARTER C. COLLINS,; FRANK A. SAUNDERS,; BENJAMIN WHITE ...
[16]
Dendritic Spine Plasticity: Function and Mechanisms - Frontiers
Dendritic spines are small protrusions studding neuronal dendrites, first described in 1888 by Ramón y Cajal using his famous Golgi stainings.
[17]
Structural and functional plasticity of dendritic spines - NIH
It is clear that the structural plasticity of dendritic spines is related to changes in synaptic efficacy, learning and memory, and other cognitive processes.
[18]
LTP Promotes a Selective Long-Term Stabilization and Clustering of ...
Our results indicate that synaptic remodeling associated with induction of long-term potentiation favors the selection of inputs showing spatiotemporal ...
[19]
Structural changes at dendritic spine synapses during long-term ...
Aug 9, 2025 · We investigated this issue by reconstructing dendrites, axons and synapses from hippocampus during long-term potentiation (LTP) and maturation.<|separator|>
[20]
Structural plasticity of the adult brain - PMC - PubMed Central
Clear evidence that structural changes occur in the brain throughout life, including the generation of new neurons and other brain cells, and connections ...
[21]
Neural plasticity and its contribution to functional recovery - PMC
May 25, 2016 · Modification of sensory input may induce rapid changes in cortical representations through various mechanisms including unmasking of connections ...Missing: dormant | Show results with:dormant
[22]
Preclinical Studies of Neuroplasticity Following Experimental Brain ...
Aug 8, 2019 · Here, we review recent advances that have informed our understanding of neuroplasticity following experimental models of brain injury.
[23]
The presence of ineffective synapses and the circumstances which ...
The presence of ineffective synapses and the circumstances which unmask them. Patrick David Wall.
[24]
NEUROPLASTICITY: EVIDENCE FROM APHASIA - PMC - NIH
Aphasia recovery shows neuroplasticity through right hemisphere areas, undamaged left areas, and map extension, with increased blood flow in these areas.
[25]
Topographic reorganization of somatosensory cortical areas 3b and ...
In at least most cortical sectors, there was a consistent, maintained relationship between receptive field size and magnification, i.e. as representations ...
[26]
Topographic reorganization of somatosensory cortical areas 3b and ...
In at least most cortical sectors, there was a consistent, maintained relationship between receptive field size and magnification i.e. as representations ...
[27]
Donald O. Hebb and the Organization of Behavior: 17 years in the ...
Apr 6, 2020 · This book introduced the concepts of the “Hebb synapse”, the “Hebbian cell assembly” and the “Phase sequence”. The most frequently cited of ...
[28]
Long-lasting potentiation of synaptic transmission in the dentate ...
Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path ... J Physiol. 1973 ...
[29]
Long-Term Synaptic Depression - Neuroscience - NCBI Bookshelf
LTD occurs when the Schaffer collaterals are stimulated at a low rate—about 1 Hz—for long periods (10–15 minutes). This pattern of activity depresses the EPSP ...
[30]
AMPA receptor trafficking and long-term potentiation - PubMed Central
I review studies from our laboratory that support a critical role for AMPA receptor trafficking in LTP and experience-dependent plasticity.
[31]
dependence on spike timing, synaptic strength, and postsynaptic ...
1998 Dec 15;18(24):10464-72. doi: 10.1523/JNEUROSCI.18-24-10464.1998. Authors. G Q Bi , M M Poo. Affiliation. 1 Department of Biology, University of ...
[32]
Synaptic plasticity and memory: an evaluation of the hypothesis
The synaptic plasticity and memory hypothesis states that activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation.
[33]
Conceptualizing functional neuroplasticity - PubMed - NIH
Cross-modal reassignment occurs when structures previously devoted to processing a particular kind of sensory input now accepts input from a new sensory method.
[34]
Increased cortical representation of the fingers of the left hand in ...
Science. 1995 Oct 13;270(5234):305-7. doi: 10.1126/science.270.5234.305. Authors. T Elbert , C Pantev, C Wienbruch, B Rockstroh, E Taub. Affiliation. 1 ...
[35]
Molecular mechanisms of experience-dependent plasticity in visual ...
Experience-dependent plasticity embodies the developmental history of the organism and matches neuronal circuits to the nature of inputs to enable appropriate ...
[36]
Lifelong Experience-Dependent Plasticity in the Sensory Cortex
It is widely accepted that plasticity is a characteristic of the young brain, enabling early experiences to exert tremendous influence over the development of ...
[37]
Experience-dependent neural plasticity in the adult damaged brain
This experience-driven plasticity is needed to respond to, and learn from, an ever-changing environment: It is the mechanism of behavioral change. Behavioral ...
[38]
Plasticity of the human auditory cortex related to musical training
As a complete review on all aspects of structural and functional plasticity through musical training is beyond the scope of this paper ... Pantev et al ...Missing: Pantev | Show results with:Pantev
[39]
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms
Aug 29, 2007 · Most forms of short-term synaptic plasticity are triggered by short bursts of activity causing a transient accumulation of calcium in ...
[40]
How the mechanisms of long-term synaptic potentiation and ...
Jan 5, 2014 · How the mechanisms of long-term synaptic potentiation and depression serve experience-dependent plasticity in primary visual cortex. Sam F ...
[41]
Learning, neural plasticity and sensitive periods - PubMed Central
The broader term “sensitive period” will be used here to refer to periods in development in which experience has unusually strong effects on brain and behavior ...
[42]
Time for new thinking about sensitive periods - Frontiers
It is also likely that experience-dependent behavioral or brain plasticity accrued during one sensitive period can serve as a scaffold on which later experience ...
[43]
Modeling the evolution of sensitive periods - ScienceDirect.com
These models investigate how mechanisms of plasticity can respond optimally to experience during an individual's lifetime. This paper discusses the central ...
[44]
Modulation of Neural Plasticity as a Basis for Stroke Rehabilitation
Aug 23, 2012 · Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodelling and contralesional pyramidal tract ...Neural Plasticity After... · Spontaneous Recovery Of... · Cortical Map RearrangementsMissing: seminal | Show results with:seminal
[45]
Role of the Contralesional vs. Ipsilesional Hemisphere in Stroke ...
Sep 20, 2017 · Neuronal reorganization may occur on both the ipsilesional and contralesional hemispheres during recovery to regain motor functionality.
[46]
Constraint-Induced Movement Therapy after Stroke - PMC
Meta-analysis showed strong evidence favoring both types of CIMT in terms of motor function, arm-hand activities and self-reported arm-hand functioning in daily ...
[47]
A Longitudinal Study of Hand Motor Recovery after Sub-Acute Stroke
We found that patients with sub-acute stroke have shown greater activity in the contralesional primary motor cortex (M1) during the affected hand's movement.Missing: neuroplasticity | Show results with:neuroplasticity
[48]
Evolution of Diaschisis in a Focal Stroke Model
Stroke produces an area of focal damage and distant areas of reduced blood flow and metabolism, termed diaschisis. Diaschisis may impair functional recovery by ...
[49]
A critical time window for recovery extends beyond one-year post ...
A systematic review of 14 studies suggested that, on average, recovery reaches a plateau at 15 wk poststroke for patients with severe hemiparesis and at 6.5 wk ...
[50]
Activation of the primary visual cortex by Braille reading in blind ...
Apr 11, 1996 · Blind subjects showed activation of primary and secondary visual cortical areas during tactile tasks, whereas normal controls showed deactiva-tion.
[51]
Visual Cortex Activity in Early and Late Blind People
May 15, 2003 · A subsequent fMRI study confirmed that tactile stimulus activation of visual cortex correlated with sensory processing because tactile ...
[52]
Mechanisms of Cross-Modal Plasticity in Early-Blind Subjects - PMC
Visual cortex activation in late-onset, Braille naive blind individuals: an fMRI study during semantic and phonological tasks with heard words. Neurosci ...
[53]
PET Evidence of Neuroplasticity in Adult Auditory Cortex of ...
Sep 1, 2003 · PET scans were performed for the deaf patient as a clinical presurgical evaluation. Sufficient and detailed explanations for the procedure ...Missing: signers | Show results with:signers
[54]
Cortical reorganization in postlingually deaf cochlear implant users
The current review aims to identify these cortical changes in postlingually deaf CI users and discusses their maladaptive or adaptive relationship to the CI ...Missing: papers | Show results with:papers
[55]
Neural Correlates of Natural Human Echolocation in Early and Late ...
Previous fMRI research has shown a contralateral bias in auditory cortex for monoaural stimulation [16]–[18]. But to date, fMRI research has not been able to ...Missing: neuroplasticity | Show results with:neuroplasticity
[56]
Changes in primary visual and auditory cortex of blind and sighted ...
Jun 4, 2024 · We found that blind participants and sighted participants together showed a training-induced increase in activation in left and right V1 in response to echoes.
[57]
Harnessing brain plasticity to improve binocular vision in amblyopia
Amblyopia treatment involves correcting refractive error to ensure clear and equal retinal image formation in both eyes, then, if necessary, promoting the use ...
[58]
Leveraging neural plasticity for the treatment of amblyopia
Insights derived from animal models about the factors that govern neural plasticity have been leveraged to develop innovative treatments for amblyopia.
[59]
Durable recovery from amblyopia with donepezil | Scientific Reports
Jun 22, 2023 · Abstract. An elevated threshold for neuroplasticity limits visual gains with treatment of residual amblyopia in older children and adults.
[60]
Speech-like cerebral activity in profoundly deaf people processing ...
Using positron emission tomography, we report cerebral blood flow activity in profoundly deaf signers processing specific aspects of sign language in key brain ...
[61]
Impact of Early Deafness and Early Exposure to Sign Language on ...
Nov 15, 2001 · This functional magnetic resonance imaging study investigated the impact of early auditory deprivation and/or use of a visuospatial language ...
[62]
A review of current theories and treatments for phantom limb pain
Jun 1, 2018 · Currently, the most commonly posited CNS theory is the cortical remapping theory (CRT), in which the brain is believed to respond to limb loss ...
[63]
Phantom limb pain, cortical reorganization and the therapeutic effect ...
We investigated 13 upper limb amputees with phantom limb pain (PLP) during hand and lip movement, before and after intensive 6-week training in mental imagery.
[64]
Synaesthesia in phantom limbs induced with mirrors - Journals
Ramachandran V. S. and; Rogers-Ramachandran D. 1996Synaesthesia in phantom limbs induced with mirrorsProc. R. Soc. Lond. B.263377–386http://doi.org/10.1098 ...
[65]
Graded motor imagery for pathologic pain: a randomized ... - PubMed
Conclusion: Motor imagery reduced pain and disability in these patients with complex regional pain syndrome type I or phantom limb pain, but the mechanism, or ...
[66]
Mirror therapy for phantom limb pain: brain changes and the role of ...
fMRI data analyses revealed a relationship between change in pain after MT and a reversal of dysfunctional cortical reorganization in primary somatosensory ...
[67]
The development of human visual cortex and clinical implications
Apr 24, 2018 · During the first 2 years of this stage (~1–3 years), children are most susceptible to abnormal binocular vision that can cause amblyopia.
[68]
Neurobiology of infant attachment: Attachment despite adversity and ...
We review recent findings related to the neurobiology of infant attachment, emphasizing the role of parenting quality in attachment formation and emotional ...Missing: neuroplasticity | Show results with:neuroplasticity
[69]
Prolonged Environmental Enrichment Promotes Developmental ...
Apr 25, 2021 · These findings indicate that protracted environmental stimulation is sufficient to modulate developmental myelination and to promote behavioral function.
[70]
Environmental influences on the pace of brain development - PMC
Some models suggest that the absence of cognitive enrichment in specific domains leads to accelerated synaptic pruning in brain regions that process complex ...
[71]
Training‐induced neuroanatomical plasticity in ADHD: A tensor ...
ADHD bears a considerable impact on brain structure and function, and converging research findings appoint the frontal lobes, striatum, and cerebellum as ...
[72]
Improving Outcomes for Youth with ADHD: A Conceptual Framework ...
Interventions combining next-generation neurocognitive training with conceptually-matched skill-based training may improve outcomes for children with ADHD.
[73]
Preventive Interventions for ADHD: A Neurodevelopmental ...
Early intervention targets the child at a time when the brain is more “plastic” and perhaps more amenable to lasting “rewiring.” Furthermore, early ...Missing: therapy | Show results with:therapy
[74]
Social influences on neuroplasticity: Stress and interventions to ...
Among the influences on brain structure and function that are most powerful in inducing plastic change are social influences. The vertebrate brain appears to be ...
[75]
Plasticity of the language system in children and adults - PMC
Overall, this work has concluded that language organization in the brain is highly plastic early in life: language abilities can develop successfully even if ...
[76]
The effect of bilingualism on brain development from early childhood ...
Bilingualism affects the structure of the brain in adults, as evidenced by experience-dependent grey and white matter changes in brain structures.
[77]
Dynamic Effects of Immersive Bilingualism on Cortical ... - Frontiers
Apr 24, 2022 · Bilingualism has been shown to induce neuroplasticity in the brain, but conflicting evidence regarding its specific effects in grey matter ...
[78]
Microstructural plasticity in the bilingual brain - ScienceDirect.com
Past neuroimaging studies have demonstrated that learning a second language (L2) induced neuroplasticity at the macrostructural level, as indexed by gray matter ...
[79]
Bilingualism: Consequences for Mind and Brain - PMC
There is some evidence for the plasticity of cortical grey matter in response to bilingualism. ... Neuroplasticity: changes in grey matter induced by training.Missing: gray seminal
[80]
A critical period for second language acquisition: Evidence from 2/3 ...
The results support the existence of a sharply-defined critical period for language acquisition, but the age of offset is much later than previously speculated.Missing: neuroplasticity | Show results with:neuroplasticity
[81]
Neuroplasticity as a function of second language learning
In this article we review emerging evidence regarding how structural neuroplasticity occurs in the brain as a result of one's bilingual experience.
[82]
Dynamic neuroplasticity of language networks - PNAS
Jul 14, 2025 · This reduction in left hemisphere dominance and increased reliance on the right hemisphere is often attributed to adaptation to rely more on ...
[83]
Functional MRI study of language organization in left-handed and ...
Aug 5, 2020 · Our objective is to compare fMRI maps for all three languages in left- and right-handed trilingual subjects. 15 right- and 15 left-handed trilingual volunteers ...
[84]
Does Bilingualism Contribute to Cognitive Reserve? Cognitive and ...
Growing scientific evidence suggests that lifelong bilingualism contributes to cognitive reserve and delays the onset of Alzheimer's disease symptoms.
[85]
Bilingualism and Cognitive Reserve: A Critical Overview and a Plea ...
Some studies on Alzheimer's disease have suggested that CR may be enhanced by life-long bilingualism. However, the evidence is inconsistent.
[86]
A neural mechanism of cognitive reserve: The case of bilingualism
Nov 1, 2023 · Our findings confirm that lifelong bilingualism is a CR factor, as bilingual older adults performed just as well as their monolingual peers on tasks of ...
[87]
Neuroplasticity subserving motor skill learning - PubMed Central - NIH
Sep 12, 2011 · Here, we review findings demonstrating functional and structural plasticity across different spatial and temporal scales that mediate motor skill learning.
[88]
Navigation-related structural change in the hippocampi of taxi drivers
Taxi drivers had a significantly greater volume in the posterior hippocampus, whereas control subjects showed greater volume in the anterior hippocampus. The ...
[89]
Neurogenesis and the spacing effect: Learning over time enhances ...
Information that is spaced over time is better remembered than the same amount of information massed together. This phenomenon, known as the spacing effect, ...
[90]
Spaced Learning Enhances Episodic Memory by Increasing Neural ...
Jul 3, 2019 · Spaced learning improves long-term memory by increasing retrieval effort and enhancing the pattern reinstatement of prior neural representations.
[91]
A Review of Human Brain Plasticity and Training-Induced Learning
This research, which has been predominantly carried out with young adults, provides compelling evidence for common principles of learning and learning transfer.
[92]
Mind over matter – what do we know about neuroplasticity in adults?
We identified 36 studies, employing training as variable as juggling, working memory, meditation, learning abstract information, and aerobic exercise.
[93]
Effects of Physical Exercise on Neuroplasticity and Brain Function
Dec 14, 2020 · Physical exercise (PE) has been associated with increase neuroplasticity, neurotrophic factors, and improvements in brain function.
[94]
Exercise-Mediated Neurogenesis in the Hippocampus via BDNF
The present review synthesizes the extant literature detailing the relationship between exercise and hippocampal neurogenesis, and identifies a key molecule ...
[95]
Comparative overview of the effects of aerobic and resistance ...
The effects of aerobic exercise on neuroplasticity have been extensively studied in humans, including improvement of cognition/mood and hippocampal volume ...Material And Methods · Exercise Paradigms · Aerobic Protocol On A...<|control11|><|separator|>
[96]
Functional and/or structural brain changes in response to resistance ...
Jul 10, 2019 · Based on our analyses, resistance exercises and resistance training evoked substantial functional brain changes, especially in the frontal lobe, ...
[97]
Physical activity and neuroplasticity in neurodegenerative disorders
Feb 28, 2025 · Aerobic exercise was found to increase hippocampal volume by 1–2% and improve executive function scores by 5–10% in older adults. Resistance ...
[98]
Physical Activity to Counter Age-Related Cognitive Decline: Benefits ...
May 17, 2025 · Aerobic exercise also induces vasodilation, resulting in increased blood flow to cerebral regions, which may improve cognitive function by ...
[99]
Meditation experience is associated with increased cortical thickness
Previous research indicates that long-term meditation practice is associated with altered resting electroencephalogram patterns.
[100]
Meditation and yoga practice are associated with smaller right ... - NIH
Feb 7, 2018 · In the present study, we observed that the meditation and yoga group had a smaller right amygdala. Stress reduction has been associated with ...
[101]
Mindfulness practice leads to increases in regional brain gray matter ...
Recently, several cross-sectional anatomical MRI studies have demonstrated that experienced meditators exhibit a different gray matter morphometry in multiple ...
[102]
Psilocybin-assisted mindfulness training modulates self ... - PubMed
Aug 1, 2019 · Psilocybin-assisted mindfulness training modulates self-consciousness and brain default mode network connectivity with lasting effects.Missing: 2023-2025 | Show results with:2023-2025
[103]
Attention and Default Mode Network Assessments of Meditation ...
Meditators demonstrated increased magnitude of differential activation in the dorsal attention vs. default mode network in a sustained attention task, relative ...
[104]
[PDF] increased corpus callosum size in musicians
Since anatomic studies have provided evidence for a positive correlation between midsagittal callosal size and the number of fibers crossing through the CC, ...<|control11|><|separator|>
[105]
Music Making as a Tool for Promoting Brain Plasticity across the Life ...
Moreover, musicians who began training at an early age (≤7 years) had a significantly larger corpus callosum compared to musicians who started later (Fig.
[106]
(PDF) Morphology of Heschl's gyrus reflects enhanced activation in ...
Aug 10, 2025 · These results indicate that both the morphology and neurophysiology of Heschl's gyrus have an essential impact on musical aptitude.
[107]
Musical Training as a Framework for Brain Plasticity: Behavior ...
Nov 8, 2012 · A computational model of mechanisms controlling experience-dependent reorganization of representational maps in auditory cortex. Cogn. Affect ...Missing: seminal paper
[108]
A conceptual framework for a neurophysiological basis of art therapy ...
This conceptual paper aims to inform the neurophysiological rationale for the use of art therapy as a therapeutic approach for individuals with PTSD.
[109]
Effectiveness of Trauma-Focused Art Therapy (TFAT) for ...
The TFAT protocol led to a clinically significant reduction in PTSD symptoms. •. Art therapy reduced depression and enhanced emotional articulation. •. Art ...
[110]
Musicians and music making as a model for the study of brain plasticity
Cross-sectional studies have shown that musically trained children are better than musically untrained children on a range of auditory and motor abilities, such ...
[111]
Drawing enhances cross-modal memory plasticity in the human brain
The results reveal the operation of a rapid training-based plasticity mechanism that recruits the resources of V1 in the process of learning to draw.<|control11|><|separator|>
[112]
Age-Related Changes in Cognition, Plasma Levels of Brain-Derived ...
Aug 4, 2025 · There was significant reduction in cognitive score and plasma levels of BDNF as decades of life increased. The cognitive scores were ...
[113]
Compensatory cognition in neurological diseases and aging
In this review, we are highlighting the events of structural and functional recovery and compensatory cognitive ability after the loss of the principal network.
[114]
Amyloid β-based therapy for Alzheimer's disease - Nature
Jun 30, 2023 · Although Aβ aggregates, especially the soluble oligomeric species impair synaptic plasticity by inhibition of LTP and induction of LTD, growing ...
[115]
Amyloid-β Induced Neuronal Dysfunction in Alzheimer's Disease
Dysregulation of Aβ in Alzheimer's disease could override these activity-dependent synaptic mechanisms, leading to synaptic failure and cognitive decline.
[116]
Neurophysiological markers of motor compensatory mechanisms in ...
Aug 27, 2024 · The hypothesis that motor compensatory mechanisms in PD reflect adaptations of motor networks despite the increasing neurodegenerative burden ...Neurophysiological Markers... · Tms Techniques And Emg... · Corticospinal Excitability...<|control11|><|separator|>
[117]
Neuroplasticity in Parkinson's disease | Journal of Neural ...
Aug 5, 2024 · Neuroplasticity is a fundamental property of the human brain to adapt both to external changes and internal insults and pathological processes.
[118]
Neural Plastic Effects of Cognitive Training on Aging Brain - PMC - NIH
Cognitive training can possibly ameliorate age-associated cognitive decline by inducing training-specific neural plastic changes at both neural and behavioral ...
[119]
The ACTIVE Study: Study Overview and Major Findings - PMC
The ACTIVE study is the first large-scale, randomized trial to test the long-term outcomes of cognitive training effects on prevention of decline in daily ...Missing: neuroplasticity | Show results with:neuroplasticity
[120]
UCSD Alzheimer's Disease Clinical Trials for 2025 — San Diego
Oct 19, 2025 · This is a first-in-human clinical trial to test whether a protein administered into the brain continuously by gene therapy, Brain-Derived ...Missing: neuroplasticity | Show results with:neuroplasticity
[121]
Alzheimer's gene therapy shows promise in preserving brain function
Jun 9, 2025 · Researchers at University of California San Diego School of Medicine have developed a gene therapy for Alzheimer's disease (AD) that could help protect the ...Missing: neuroplasticity | Show results with:neuroplasticity
[122]
hippocampal neurons in adult mice living in an enriched environment
Apr 3, 1997 · Here we show that significantly more new neurons exist in the dentate gyrus of mice exposed to an enriched environment compared with littermates ...
[123]
Environmental enrichment requires adult neurogenesis to facilitate ...
Mar 23, 2010 · The survival of newly born hippocampal neurons is decreased by chronic psychosocial stress and increased by exposure to enriched environments.
[124]
Traumatic brain injury promotes neurogenesis at the cost of ... - Nature
Jun 18, 2024 · We show that TBI modifies NSC fate to promote neurogenesis at the cost of astrogliogenesis and identify specific cell populations as possible targets.
[125]
Questioning Seasonality of Neuronal Plasticity in the Adult Avian Brain
Jul 26, 2018 · A prominent example is the song control system in the avian brain, where seasonal changes in song behavior are accompanied by changes in the ...
[126]
Brain-wide neural dynamics of poststroke recovery induced by ...
Aug 11, 2021 · Poststroke optogenetic stimulations can promote functional recovery. However, the circuit mechanisms underlying recovery remain unclear.
[127]
[PDF] TRANSHUMANISM, BRAIN-COMPUTER INTERFACES, AND ...
This thesis explores the intersection of transhumanism, brain-computer interfaces (BCIs), and the ethical implications of selective perfectibility. It examines ...
[128]
Using brain–computer interfaces to induce neural plasticity and ...
Unfortunately, the properties of BCI systems that are potentially relevant for inducing neural plasticity can often not be optimized independently.
[129]
https://www.nature.com/articles/s41467-024-49299-6
[130]
https://pmc.ncbi.nlm.nih.gov/articles/PMC7259116/
[131]
The dark side of neuroplasticity - PMC - PubMed Central - NIH
These dysfunctions are caused, at least in part, by an imbalance of inhibitory and excitatory synaptic inputs to spinal neurons and several relate to a loss of ...
[132]
Maladaptive plasticity in tinnitus — triggers, mechanisms and ...
Feb 12, 2016 · Maladaptive neural plasticity seems to underlie these changes: it results in increased spontaneous firing rates and synchrony among neurons in central auditory ...
[133]
Maladaptive plasticity in tinnitus-triggers, mechanisms and treatment
Jun 7, 2016 · Maladaptive neural plasticity appears to underlie these neural changes, as it results in increased spontaneous firing rates and synchrony among ...
[134]
Neuroplasticity in addictive disorders - PMC - PubMed Central - NIH
Addiction is a disease of neuroplasticity, where the reward system is activated by cues, leading to a drive to resume drug-taking. This is a memory trace.
[135]
Plasticity of Addiction: a Mesolimbic Dopamine Short-Circuit? - NIH
Addiction occurs because drugs of abuse are able to take control of normal brain reward circuits that provide reinforcement of behaviors related to survival.
[136]
Neuropathic Pain: A Maladaptive Response of the Nervous System ...
Neuropathic pain is triggered by lesions to the somatosensory nervous system that alter its structure and function so that pain occurs spontaneously.
[137]
Neuroplasticity in chronic pain: insights into diagnosis and treatment
Apr 1, 2025 · This review highlights neuro-plastic changes in chronically painful patients and acknowledges the brain's plasticity as a target for chronic ...
[138]
Neuroplasticity to a Single-episode Traumatic Stress Revealed by ...
Our data provide neuroimaging evidence suggesting that prolonged neuroadaptation induced by a single episode of traumatic stress can be non-invasively detected ...
[139]
Fear Conditioning, Synaptic Plasticity, and the Amygdala
Evidence from animal models and human neuroimaging studies suggest that one of the underlying mechanisms of PTSD may be aberrant synaptic plasticity. Synaptic ...Missing: maladaptive | Show results with:maladaptive
[140]
A Rodent Model of Exposure Therapy: The Use of Fear Extinction as ...
Mar 11, 2019 · Extinction is a learning process that promotes plasticity in the mPFC. Extinction learning activates the mPFC, much like exposure therapy in ...Fear Extinction As A... · Extinction Learning Reverses... · Figure 1
[141]
Erasing “bad memories”: reversing aberrant synaptic plasticity as ...
Apr 10, 2025 · In this review, we propose that preventing or reversing such maladaptive synaptic strengths and erasing such aberrant “memories” could be a disease-modifying ...L-Dopa-Induced Dyskinesia... · Targeting Synaptic... · Molecular Targets To...<|control11|><|separator|>
[142]
Critical period regulation across multiple timescales - PNAS
Jun 5, 2020 · Here, we consider recent progress in the biological basis of critical periods as a unifying rubric for understanding plasticity across multiple timescales.Critical Period Regulation... · Abstract · Parvalbumin Circuits As A...
[143]
Roles for Sleep in Neural and Behavioral Plasticity - Frontiers
Short periods of sleep loss decrease the number of dendritic spines in the CA1 region of the hippocampus due to increased activity of the actin-binding protein ...
[144]
The critical periods of cerebral plasticity: A key aspect in a dialog ...
“Critical periods” of cerebral development represent temporal windows that mark favorable, but also circumscribed, moments in developmental cerebral plasticity.Critical periods as temporal... · dialog between... · The reopening and reclosing...Missing: seminal papers
[145]
https://pmc.ncbi.nlm.nih.gov/articles/PMC4253640/
[146]
https://pmc.ncbi.nlm.nih.gov/articles/PMC3206195/
[147]
https://pmc.ncbi.nlm.nih.gov/articles/PMC6421316/
[148]
New AI-based method reduces latency in neurofeedback by 50-fold
Oct 12, 2023 · The results were obtained by employing a neural network trained in low-latency filtering of brain activity signals from diverse individuals.Missing: personalized advances
[149]
AI-Driven Neurofeedback: Changing Human Thought Processes
This article explores the evolving relationship between AI and neurofeedback, focusing on how AI-driven systems can optimize brain function, improve mental ...
[150]
Channeling Seizure Control: Optogenetics in Human Brain Slices
Apr 13, 2025 · Here we demonstrate adeno-associated virus-mediated, optogenetic reductions in network firing rates of human hippocampal slices recorded on high-density ...Missing: neuroplasticity | Show results with:neuroplasticity
[151]
https://www.frontiersin.org/journals/molecular-neuroscience/articles/10.3389/fnmol.2022.1057539/full
[152]
Mapping brain changes in post-COVID-19 cognitive decline via FDG ...
Jul 2, 2025 · Cognitive decline is a common symptom of post-COVID-19 syndrome. However, the mechanisms underlying this deficit remain poorly understood.Missing: neuroplasticity haul
[153]
Neurological symptoms in Long COVID patients persist up to three ...
Aug 15, 2024 · Among the most significant findings, the symptoms of 'brain fog,' characterized by cognitive dysfunction, was experienced by 60% of patients and ...Missing: neuroplasticity | Show results with:neuroplasticity
[154]
Research Report Persistent neurocognitive deficits in long COVID
These findings indicate that even mild COVID-19 can result in persistent neurocognitive deficits, structural brain alterations, and functional network ...Missing: neuroplasticity | Show results with:neuroplasticity
[155]
Sex differences in patterns of white matter neuroplasticity after ...
These data support a growing body of evidence suggesting that females exhibit increased WM neuroplasticity changes relative to males despite comparable changes ...
[156]
https://www.researchgate.net/publication/386172428_AI-Driven_Neurofeedback_Changing_Human_Thought_Processes
[157]
Digital Media and Developing Brains: Concerns and Opportunities
Mar 4, 2024 · Effects of digital media may begin when brain networks are developing quickly and plasticity is high. Additionally, sex differences may ...
[158]
https://doi.org/10.1038/s41593-024-01782-5