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Plasticity

Plasticity denotes the capacity of certain materials, biological systems, or neural structures to undergo non-reversible deformation or reorganization under stress, experience, or environmental variation, without immediate rupture or loss of viability.^[1]^[2]^[3] In materials science and physics, plasticity manifests as the permanent reshaping of solids, such as metals, when stressed beyond their elastic limit, enabling applications in manufacturing and engineering while governed by mechanisms like dislocation motion.^[1]^[4] This property contrasts with elasticity, where recovery occurs, and empirical tests reveal yield points beyond which strain hardening or necking ensues.^[4] In biology, phenotypic plasticity allows a fixed genotype to express variable traits—such as altered morphology or physiology—in response to ecological cues, facilitating short-term adaptation without genetic mutation, as documented in studies of plant leaf responses or animal development.^[2]^[5] Key evidence includes reaction norms, where trait expression shifts predictably with conditions, though costs like reduced fitness in mismatched environments limit its scope.^[6] In neuroscience, neuroplasticity encompasses structural rewiring, synaptic strengthening (e.g., via long-term potentiation), and functional remapping, driven by experience or injury, underpinning learning and recovery but diminishing with age due to reduced synaptic turnover.^[7]^[3] Notable achievements include rehabilitation outcomes post-stroke, where targeted training induces cortical reorganization, yet controversies persist over exaggerated claims of boundless malleability, as causal mechanisms reveal genetically constrained critical periods and incomplete restitution.^[8]^[9] Across domains, plasticity underscores causal realism in adaptation, with empirical models emphasizing thresholds, energy costs, and reversibility limits over unbounded flexibility.^[10]^[4]

Materials Science

Definition and Fundamental Principles

Plasticity in materials science denotes the capacity of a solid material to experience permanent, non-reversible deformation under sufficient applied stress, without fracturing, in contrast to elastic deformation that fully recovers upon stress removal. This behavior emerges beyond the material's elastic limit, where atomic bonds stretch or break, allowing reconfiguration of the microstructure.^[11] The onset of plasticity is marked by the yield strength, defined as the stress threshold initiating appreciable permanent strain, typically measured via tensile testing where the stress-strain curve deviates from linearity.^[12] For metals, yield strengths vary widely; for example, annealed low-carbon steel exhibits around 250 MPa, while high-strength alloys like titanium can exceed 800 MPa under room temperature conditions. At the fundamental level, plastic deformation in crystalline materials primarily proceeds through dislocation motion, where line defects in the crystal lattice glide under shear stress, enabling shear on specific crystallographic planes without requiring the high energy of perfect lattice sliding. Dislocations, first theoretically proposed by Taylor, Orowan, and Polanyi in 1934, lower the Peierls-Nabarro stress barrier for deformation, allowing strains as low as 0.1% to initiate yielding in pure metals.^[13] This glide occurs along defined slip systems, comprising a close-packed plane (e.g., {111} in face-centered cubic crystals) and a close-packed direction (e.g., <110>), with the resolved shear stress on a system given by Schmid's law: \tau = \sigma \cos\phi \cos\lambda, where \sigma is applied stress, \phi the angle to the slip plane normal, and \lambda to the slip direction.^[14] Materials with fewer active slip systems, such as hexagonal close-packed structures (often 3 basal systems), exhibit limited ductility and may deform via twinning or fracture instead.^[15] The multiplicity of slip systems governs polycrystalline ductility per the von Mises criterion, requiring at least five independent systems for arbitrary shape changes without cracking, as insufficient systems lead to strain incompatibilities at grain boundaries.^[13] Temperature and strain rate influence these principles: elevated temperatures activate climb (diffusion-mediated dislocation bypass of obstacles), enhancing ductility, while high rates suppress it by limiting dislocation mobility. Work hardening, a key consequence, arises from dislocation multiplication and interactions (e.g., forest dislocations impeding glide), increasing yield strength progressively during deformation, as quantified by the Taylor relation \sigma = \sigma_0 + \alpha Gb\sqrt{\rho}, where \rho is dislocation density, G shear modulus, b Burgers vector, and \alpha a constant around 0.3-0.5.^[16] These mechanisms underpin applications like metal forming, where controlled plasticity shapes components without failure.

Deformation Mechanisms

In crystalline materials, plastic deformation primarily occurs through the motion of dislocations, line defects in the crystal lattice that enable shear under applied stress without breaking atomic bonds. Dislocation glide, the dominant mechanism in metals at ambient temperatures, involves dislocations moving on specific crystallographic planes (slip planes) in directions dictated by the Burgers vector, following Schmid's law where resolved shear stress τ = σ cosφ cosλ exceeds the critical resolved shear stress (CRSS). For face-centered cubic (FCC) metals like aluminum, slip systems are {111}<110>, providing high ductility due to multiple active systems (up to 12), whereas body-centered cubic (BCC) metals like iron exhibit {110}<111> and {211}<111> systems with temperature-dependent CRSS influenced by lattice friction (Peierls stress). Twinning, another key mechanism, produces mirror-image lattice regions across a twin boundary, activated when slip is restricted, such as in hexagonal close-packed (HCP) metals like titanium with limited slip systems ({0001}<11-20>). Deformation twinning conserves volume but introduces orientation changes, contributing to strain hardening; in magnesium alloys, twin boundaries act as barriers to further dislocation motion, enhancing strength but reducing ductility at room temperature. Unlike slip, twinning is polar and stress-direction dependent, with nucleation at grain boundaries or defects. At elevated temperatures or low stresses, diffusional mechanisms dominate, including Nabarro-Herring creep (lattice diffusion) and Coble creep (grain boundary diffusion), where atomic migration accommodates deformation without dislocations. Nabarro-Herring creep rate ε̇ ∝ (σ/μ)(D_L Ω / d² kT), with D_L as lattice diffusivity, d grain size, Ω atomic volume, μ shear modulus, and kT thermal energy, is prevalent in fine-grained ceramics like alumina above 0.5 T_m (melting temperature). These mechanisms explain superplasticity in alloys like Ti-6Al-4V, where grain boundary sliding coupled with diffusion enables elongations >1000% at 900–950°C and strain rates ~10^{-3} s^{-1}. In amorphous materials like metallic glasses and polymers, plastic deformation lacks dislocations, relying instead on shear transformation zones (STZs)—localized regions of cooperative atomic rearrangements. In bulk metallic glasses (BMGs), such as Zr-based Vitreloy, deformation proceeds via heterogeneous STZ activation leading to serrated flow (pop-in events) and shear bands, with propensity for catastrophic failure unless nanocrystallization or heterogeneity stabilizes flow. Polymers exhibit viscoelastic mechanisms, including chain slip and disentanglement, governed by the glass transition temperature T_g; below T_g, brittle deformation via crazing occurs, while above, rubbery flow enables large strains.

Modeling and Computational Advances

Crystal plasticity finite element methods (CPFEM) have become a cornerstone for simulating anisotropic plastic deformation in polycrystalline metals, incorporating explicit consideration of crystallographic slip systems and grain orientations to predict texture evolution and strain localization.^[17] These models solve equilibrium and compatibility equations variationally, enabling detailed analysis of deformation heterogeneity at the mesoscale.^[17] Recent developments in CPFEM include multiscale integrations with molecular dynamics simulations, where atomistic insights into dislocation behaviors inform higher-scale plasticity parameters, as demonstrated in models for investigating creep mechanisms in alloys.^[18] Efficiency enhancements have arisen through fast Fourier transform (FFT)-based solvers, such as the large-strain elasto-viscoplastic FFT approach, which improves accuracy in quantifying dislocation density effects and reduces computational cost compared to traditional finite element discretizations.^[19] Additionally, finite difference-based stress integration algorithms have been proposed for CPFEM, offering robust handling of large deformations in rate-dependent viscoplastic frameworks.^[20] Multiscale modeling frameworks bridge atomic, dislocation, and continuum levels to capture plastic deformation processes in metals, with crystal plasticity models linking microscopic slip to macroscopic yield behavior.^[21] For instance, hierarchical approaches couple discrete dislocation dynamics with continuum crystal plasticity, enabling predictions of strain gradients and internal stresses in single crystals like aluminum.^[22] These methods have advanced understanding of thermally activated dislocation motion in body-centered cubic metals, such as molybdenum, by parameterizing mesoscale models from 0 K atomistic glide simulations.^[23] Machine learning has emerged as a transformative tool for data-driven plasticity modeling, bypassing traditional phenomenological assumptions to discover constitutive relations directly from experimental or simulated data. In 2022, neural networks were used to infer three-dimensional yield surfaces for metals without requiring stress-strain data, relying instead on microstructural features and achieving predictions within 5% error for validated alloys.^[24] Deep learning architectures have predicted path-dependent plasticity in metals, capturing history effects in stress-strain responses with accuracy surpassing classical models like J2 plasticity, as shown in benchmarks on FCC polycrystals.^[25] Hybrid approaches, such as proper orthogonal decomposition combined with feedforward neural networks, have accelerated simulations of anisotropic plasticity by reducing dimensionality while preserving fidelity in texture evolution predictions.^[26] These ML-enhanced models facilitate rapid prototyping of alloy behaviors under complex loading, with applications in titanium-aluminum systems for aerospace components.^[27]

Biology

Phenotypic Plasticity

Phenotypic plasticity refers to the capacity of a single genotype to produce multiple distinct phenotypes in response to varying environmental conditions, enabling organisms to adjust their traits without genetic alterations.^[2] This phenomenon encompasses changes in morphology, physiology, behavior, or life history traits, often manifesting as a continuous range of responses described by a reaction norm—the function relating environmental variation to phenotypic output.^[28] Unlike fixed genetic determination, plasticity allows for rapid adaptation to short-term fluctuations, such as seasonal changes or predation pressures, though it may incur metabolic costs or risks of maladaptive responses.^[29] The concept traces its roots to early observations of environmental influences on development, with Charles Darwin noting in 1859 how variation in traits like plant form could arise from habitat differences, laying groundwork for understanding non-genetic variability in evolution.^[30] By the mid-20th century, the term "phenotypic plasticity" gained prominence in developmental biology, initially focusing on morphological shifts but expanding to include reversible and irreversible modifications across taxa.^[5] Empirical studies, such as those on Daphnia water fleas altering helmet-like structures in predator presence, demonstrate plasticity's prevalence in both plants and animals, with reaction norms quantifiable via controlled experiments exposing clones to gradients like temperature or nutrient levels.^[31] Plasticity's adaptive value lies in buffering against environmental heterogeneity, potentially enhancing survival and reproduction; for instance, a 2018 analysis showed that plastic genotypes outperform rigid ones in fluctuating habitats by matching phenotypes to local optima.^[29] However, its expression is constrained by genetic architecture, developmental timing, and potential mismatches, as evidenced in cases where plasticity fails under novel stressors, underscoring that while widespread—observed in over 90% of studied species—it does not universally confer fitness benefits without evolutionary tuning.^[32] Quantitative models, including those integrating plasticity into population dynamics, reveal it can stabilize coexistence in competitive communities by reducing niche overlap.^[33]

Mechanisms and Evolutionary Implications

Phenotypic plasticity manifests through developmental mechanisms that produce irreversible trait changes during ontogeny in response to environmental cues, often mediated by hormonal signaling pathways. For example, in aphids and crickets, juvenile hormone levels triggered by population density cues regulate the development of winged versus wingless morphs, enabling dispersal under crowding conditions.^[28] These processes involve genotype-by-environment interactions that shape reaction norms, where the same genotype yields varying phenotypes across environmental gradients. In contrast, phenotypic flexibility enables reversible adjustments in mature organisms, such as metabolic rate shifts in response to temperature or behavioral modifications like increased foraging efficiency under resource scarcity, facilitated by rapid physiological feedback loops including enzyme induction and ion channel modulation.^[28] Mechanisms distinguish between passive plasticity, which arises directly from environmental impacts like nutrient deficits causing stunted growth, and active, anticipatory plasticity, where predictive cues—such as herbivore damage inducing plant chemical defenses—activate regulatory networks for preemptive trait expression.^[28] Molecular underpinnings include environment-sensitive gene regulation, with transcription factors and signaling cascades altering expression profiles; epigenetic factors like DNA methylation can stabilize these changes, sometimes transmitting them transgenerationally without altering DNA sequence. Detection of cues occurs via sensory receptors, followed by signal transduction that determines the speed and accuracy of phenotypic shifts, with faster responses favored in rapidly changing environments.00225-2) Evolutionarily, phenotypic plasticity buffers fitness against environmental heterogeneity, allowing populations to persist in novel or fluctuating conditions and potentially accelerating adaptation by providing a "bridge" to genetic evolution, as posited in the Baldwin effect where plastic phenotypes initially sustain viability until selection favors underlying genetic variants.^[34] This can lead to genetic accommodation, refining initially plastic traits into canalized, genetically fixed forms over generations. However, plasticity imposes costs, including maintenance expenses and risks of mismatch when cues prove unreliable, which may lower mean fitness compared to non-plastic genotypes; empirical assays, such as long-term bacterial evolution experiments, often find these costs negligible in stable contexts but evident in complex traits like immunity.^[28] ^[31] High plasticity can constrain evolutionary divergence by decoupling phenotypic from genetic variation, reducing selection on underlying loci and impeding local adaptation or speciation in divergent habitats.^[35] Its adaptive value hinges on environmental predictability: in cue-reliable, variable settings, plasticity enhances evolutionary potential by exposing cryptic genetic variation to selection, whereas in unpredictable regimes, limits like suboptimal trait production hinder progress, potentially increasing extinction risk during lags in response. Theoretical models and meta-analyses indicate plasticity evolves under relaxed or variable selection but faces barriers from low heritable variation for reaction norms, emphasizing its role as a short-term stabilizer rather than a universal driver of long-term evolution.^[31] ^[36]

Examples in Plants and Animals

In plants, phenotypic plasticity manifests in adaptive morphological changes to environmental cues such as light quality and nutrient availability. For instance, Arabidopsis thaliana seedlings exposed to shade or enriched far-red light exhibit elongated petioles and upward leaf movement (hyponasty), which positions leaves to better compete for sunlight; this response is mediated by phytochrome signaling and is reversible upon return to full light.^[37] Similarly, common bean (Phaseolus vulgaris) reduces root secondary growth under phosphorus limitation, reallocating resources to primary roots and fine roots to enhance nutrient foraging efficiency, as demonstrated in controlled experiments measuring root architecture across soil phosphate gradients.^[38] In response to crowding or neighbor detection, many herbaceous plants elongate stems to overtop competitors, a plasticity observed in species like Solanum carolinense, where internode extension increases under high-density conditions to improve access to light, though this can incur costs in mechanical stability.^[39] These plastic adjustments, quantified via reaction norms comparing trait values across densities, often enhance fitness in heterogeneous field environments but may lead to maladaptive overgrowth in uniform settings.^[40] In animals, Daphnia water fleas exemplify predator-induced plasticity, developing elongated helmets, tail spines, and larger bodies when exposed to chemical cues (kairomones) from fish predators; this morphological shift, inducible within one generation, reduces predation risk by increasing body size and gape-limited handling time, with experimental assays confirming up to 50% survival gains in defended morphs.^[41] ^[42] The response involves hormonal regulation, such as juvenile hormone analogs, and shows genetic variation in plasticity magnitude across clones, enabling rapid adaptation to fluctuating predation pressures without genetic change.^[43] Amphibian larvae, such as spadefoot toads (Spea multiplicata), display plasticity in feeding structures and body form based on pond hydroperiod; in temporary pools, they accelerate metamorphosis and develop carnivorous mouthparts and shovel-like limbs for faster development and dispersal, contrasting with omnivorous, slower-growing forms in permanent habitats, as evidenced by common garden experiments tracking development times and trait shifts under simulated drying cues.^[2] This environmentally cued divergence, driven by thyroid hormone sensitivity, boosts survival in ephemeral environments but trades off growth in stable ones. Camouflage plasticity, seen in cephalopods like octopuses, involves rapid neural-controlled skin texture and color changes via chromatophores to match substrates, enhancing crypsis against visual predators; physiological studies quantify response speeds under 1 second, linking it to conserved neural circuits across species.^[44]

Neuroscience and Psychology

Neuroplasticity Overview

Neuroplasticity, also termed neural or brain plasticity, denotes the brain's inherent capacity to reorganize its structure, functions, and connections in response to intrinsic or extrinsic factors such as experience, learning, sensory input, injury, or disease. This process encompasses adaptive modifications at multiple scales, including synaptic strengthening or weakening (long-term potentiation and depression), dendritic spine remodeling, axonal sprouting, and, in select regions like the hippocampus, the generation of new neurons via neurogenesis.^[3]^[45] Unlike earlier doctrines positing a largely static adult brain post-development, empirical observations from electrophysiological recordings, histological analyses, and neuroimaging techniques like functional MRI affirm plasticity's persistence across the lifespan, albeit with quantitative declines in efficacy beyond critical developmental windows.^[46]^[47] The foundational recognition of plasticity traces to early 20th-century formulations, with psychiatrist Adolf Meyer in 1902 characterizing the nervous system as an "apparatus of biological plasticity," emphasizing its dynamic responsiveness over rigid localizationism. Pivotal mid-20th-century experiments, such as those by Hubel and Wiesel on visual cortical reorganization in kittens (1963–1970s), revealed experience-dependent mapping changes, challenging Santiago Ramón y Cajal's 1890s assertion of immutable mature neurons. Subsequent primate studies by Michael Merzenich in the 1970s–1980s demonstrated somatosensory cortical remapping after peripheral nerve manipulation, providing direct evidence of adult malleability.^[48]^[9] In humans, plasticity manifests in clinical contexts like post-stroke recovery, where ipsilesional hemisphere recruitment and contralesional inhibition correlate with motor improvements observed via PET and fMRI; for instance, constraint-induced movement therapy leverages this to expand cortical representations by up to 2–3 times in affected areas within weeks. Learning paradigms, such as acquiring a second language or musical skills, induce measurable volumetric increases in gray matter density, as quantified in longitudinal voxel-based morphometry studies. However, plasticity exhibits directionality: while adaptive in rehabilitation—evidenced by phantom limb alleviation through mirror therapy—maladaptive forms contribute to chronic pain or tinnitus via aberrant central sensitization.^[49]^[50]^[47] These findings, drawn from controlled trials and meta-analyses, underscore plasticity's causal role in behavioral adaptation but highlight its modulation by factors like age, genetics, and neurotrophic factors such as BDNF, whose expression declines by approximately 50% from young adulthood to senescence.^[51]

Structural and Functional Changes

Structural neuroplasticity refers to physical modifications in neural architecture, such as the formation of new synapses (synaptogenesis), remodeling of dendritic spines, and axonal sprouting, which support adaptive responses to environmental demands or injury. These changes occur throughout life but are more pronounced during development and in response to intense stimuli; in adults, they are evidenced by increases in dendritic spine density following sensory experience, where spines—protrusions hosting the majority of excitatory synapses—undergo actin-driven growth and stabilization linked to synaptic strengthening via mechanisms like long-term potentiation (LTP).^[52]^[53]^[54] In the adult mammalian cortex, targeted stimulation, such as whisker activation in rodents, induces synaptogenesis primarily on dendritic shafts and spines, shifting inhibitory and excitatory synapse distributions to refine circuit specificity.^[55] Human imaging studies, including magnetic resonance imaging (MRI), detect corresponding gray matter volume increases in regions like the hippocampus after spatial navigation training, reflecting dendritic arborization and synaptogenesis, though such volumetric shifts may partly arise from gliosis or vascular changes rather than pure neuronal growth.^[3]^[56] Axonal sprouting contributes to structural rewiring, particularly post-injury, where undamaged neurons extend projections to reconnect circuits; for instance, after cortical lesions, sprouting from nearby intact axons can restore connectivity, as observed in animal models of stroke via anterograde tracing.^[57] Neurogenesis, the birth of new neurons, plays a limited role in adult structural plasticity, confined mainly to the hippocampus and olfactory bulb, with integration into circuits aiding memory but not broadly compensating for widespread damage.^[50] These structural adaptations are activity-dependent and modulated by factors like neurotrophins (e.g., BDNF), which promote spine formation but require repeated stimuli for persistence, underscoring that changes are not indefinite but stabilize based on ongoing use.^[53] Functional neuroplasticity manifests as reorganization of neural activity and connectivity without necessarily altering gross anatomy, enabling remapping where surviving brain areas assume roles of impaired ones. Post-traumatic brain injury (TBI), functional magnetic resonance imaging (fMRI) reveals upregulation of synaptic markers weeks after onset, facilitating cortical remodeling and shifts in activation from contralateral to ipsilateral hemispheres for motor recovery.^[57]^[58] In skill learning, such as musical training, positron emission tomography (PET) and fMRI demonstrate initial widespread recruitment narrowing to specialized networks, with cross-modal plasticity—e.g., visual cortex repurposed for auditory processing in the deaf—evidenced by altered evoked responses in early sensory deprivation cases.^[59]^[60] White matter tracts also exhibit functional plasticity, with diffusion tensor imaging showing enhanced fractional anisotropy in tracts like the corticospinal pathway after rehabilitation, indicating myelination or axonal integrity improvements that support faster signal propagation.^[56] These structural and functional changes often interplay; for example, LTP-induced spine enlargement correlates with enhanced functional efficacy, as measured by increased postsynaptic currents, while maladaptive remapping—such as phantom limb pain from cortical invasion by adjacent representations—highlights plasticity's double-edged nature, where unguided reorganization can perpetuate dysfunction without targeted intervention.^[61]^[58] Longitudinal studies confirm that exercise augments both, boosting hippocampal volume via structural neurogenesis and improving inter-regional connectivity via functional synchronization, with effects quantifiable in older adults showing delayed cognitive decline.^[62]^[63] Overall, while robust in youth, adult manifestations depend on lesion size, timing, and behavioral reinforcement, with evidence from randomized trials emphasizing that plasticity-driven recovery plateaus without sustained, specific training.^[64] Neuroplasticity is constrained by developmental critical periods, during which sensory experiences are essential for circuit maturation, after which plasticity sharply diminishes, limiting the brain's adaptability in adulthood compared to childhood.^[65] These periods, such as those for visual and language processing, close as inhibitory mechanisms like GABAergic signaling strengthen, reducing the window for profound rewiring.^[66] In adults, while some plasticity persists for learning and recovery, it is less robust, with diminished capacity for synaptogenesis and dendritic remodeling, as evidenced by altered neuronal ensemble dynamics and gene expression changes like reduced Arc activity.^[67] Aging exacerbates these limits through progressive declines in key plasticity mechanisms, including reduced adult hippocampal neurogenesis, where neuronal progenitor proliferation decreases significantly, as shown in rat dentate gyrus studies from 1996 onward.^[52] Synaptic plasticity falters with impaired long-term potentiation (LTP) and long-term depression (LTD) in the hippocampus, linked to memory retrieval deficits in aged rodents, alongside losses in spine density and perforated synapses.^[52]^[67] Calcium dysregulation and increased conductance further hinder LTP induction thresholds, contributing to cognitive impairments in spatial memory and executive function within the hippocampus and prefrontal cortex, without substantial neuronal loss but with subtle dendritic alterations.^[67] Empirical evidence from non-invasive brain stimulation paradigms, reviewed across 39 studies, indicates older adults show reduced corticospinal excitability responses, particularly to paired associative stimulation, suggesting attenuated neuroplasticity induction compared to younger individuals, though variability persists.^[68] Structural changes, such as gray matter atrophy detectable within one year of healthy aging and decreased synaptic density, compound functional declines driven by oxidative stress, mitochondrial dysfunction, and neuroinflammation.^[52] These age-related reductions heighten vulnerability to cognitive decline, underscoring plasticity's finite nature despite interventions like exercise that offer partial mitigation.^[52]

Recent Research Developments

In 2024, researchers at Stanford Medicine identified molecular pathways enabling the generation of new neurons from glia cells in the adult hippocampus of mice, suggesting potential therapeutic targets for countering age-related declines in neurogenesis through pharmaceutical or genetic interventions.^[69] Concurrently, a CRISPR-Cas9 screen published in Nature pinpointed regulators of neural stem cell quiescence during ageing, revealing that disrupting specific genes like Pten and Tsc1 enhances proliferation in adult mammalian brains, with implications for restoring regenerative capacity.^[70] Pharmacological advancements have highlighted psychedelics' role in promoting structural plasticity; a 2025 review in Trends in Pharmacological Sciences detailed how psilocin, the active metabolite of psilocybin, induces sustained dendritic spine growth and synaptogenesis via intracellular 5-HT2A receptor signaling, persisting beyond acute effects and supporting antidepressant efficacy.^[71] Similarly, studies on methylone, a cathinone analog, demonstrated long-lasting increases in neurite outgrowth and dendritic spine density in preclinical PTSD models, mediated by enhanced BDNF expression and TrkB activation.^[72] Noninvasive brain stimulation techniques continue to evolve for modulating maladaptive plasticity in chronic pain; a 2025 analysis in Experimental & Molecular Medicine evaluated repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS), showing they normalize cortical hyperexcitability by facilitating Hebbian-like synaptic strengthening, with meta-analytic evidence of pain reduction in 40-60% of neuropathic patients across trials.^[73] Emerging epigenetic research underscores DNA demethylation's role in activity-dependent plasticity, as depolarization-induced demethylation at promoters like Bdnf enables transcription factor access, a mechanism conserved from in vitro models to human imaging studies.^[74] A October 2025 clinical trial reported that targeted cognitive training games elevated acetylcholine levels—a neurotransmitter tied to attention and memory—in older adults, correlating with improved executive function scores via fMRI-measured prefrontal activation, challenging prior views on fixed cholinergic declines post-maturity.^[75] These findings collectively indicate expanding windows for plasticity enhancement, though longitudinal human data remain limited, emphasizing the need for rigorous validation beyond preclinical promise.^[50]

Developmental and Resilience Contexts

Developmental Plasticity

Developmental plasticity refers to the capacity of genetically similar individuals to produce varying phenotypes in response to environmental cues encountered during early developmental stages, typically from conception to reproductive maturity.^[76] This process allows organisms to tailor traits such as morphology, physiology, and behavior to predicted future environments, often resulting in irreversible adjustments that enhance survival without requiring genetic mutations.^[77] Unlike adult phenotypic plasticity, developmental forms are constrained to ontogenetic phases where sensitivity to inputs is maximal, reflecting evolved mechanisms for matching phenotypes to heterogeneous habitats.^[76] Mechanisms underlying developmental plasticity involve gene-environment interactions, including epigenetic modifications like DNA methylation and histone alterations that alter gene expression without changing DNA sequences.^[76] Hormonal signaling pathways, such as insulin/IGF or ecdysone in invertebrates, and neural rewiring in vertebrates mediate these responses, often amplified during critical periods—discrete windows of elevated plasticity where deprivation or enrichment yields permanent outcomes.^[77]^[78] For example, in the human visual cortex, synaptic pruning and myelination peak in infancy, rendering early sensory deprivation causative of deficits like amblyopia if uncorrected by age 7-8 years.^[78] Empirical evidence from cohort studies illustrates these effects in humans: prenatal exposure to the Dutch Hunger Winter famine (1944-1945) correlated with elevated adult risks of obesity (odds ratio 1.5-2.0), cardiovascular disease, and schizophrenia, traceable to hypomethylation of IGF2 and other metabolic genes persisting into the sixth decade.^[76] Adverse childhood experiences, quantified in dose-response models, accelerate physiological aging markers like telomere shortening and elevate all-cause mortality by 20-30% in longitudinal data.^[76] In non-human animals, poor early nutrition in red deer calves (tracked 1980-2006) induced faster reproductive senescence, with affected females showing 15-20% reduced fecundity by mid-life due to constrained ovarian reserves.^[76] Social insects demonstrate nutritional polyphenism, as in honeybees where royal jelly triggers queen development via hypermethylation of vitellogenin and other genes, yielding castes differing 100-fold in size.^[77] From an evolutionary standpoint, developmental plasticity exposes latent genetic variation for selection, enabling genetic accommodation where initially plastic traits become canalized; experiments in spadefoot toads selected for predator-induced morphology shifts over 5-10 generations confirm accelerated fixation of adaptive forms.^[77]^[79] In resilience contexts, early stressors program hypothalamic-pituitary-adrenal axis hypersensitivity, diminishing adaptive capacity to later challenges—as evidenced by accelerated aging in famine-exposed cohorts—but matching adult environments can mitigate costs, aligning with predictive adaptive response models validated in primates.^[76] Limits arise post-sensitive periods, with plasticity declining due to molecular brakes like perineuronal nets in the brain, though recent findings indicate partial reactivation via pharmacological interventions in rodents.^[78]

Plasticity in Human Resilience

Plasticity in human resilience refers to the adaptive capacity of neural and behavioral systems to reorganize following exposure to stressors, facilitating recovery and maintenance of functioning despite adversity. This process underlies psychological resilience, defined as achieving positive outcomes amid challenges like trauma or chronic stress, through mechanisms such as synaptic strengthening, dendritic remodeling, and network reconfiguration in brain regions including the hippocampus and prefrontal cortex.^[80]^[81] Empirical evidence from neuroimaging studies shows that resilient individuals demonstrate greater hippocampal volume preservation and enhanced prefrontal-hippocampal connectivity compared to those developing disorders like PTSD after trauma.^[82] A key mechanism involves the plasticity of memory control circuits, where resilient responses interrupt the persistence of traumatic memories by modulating amygdala-hippocampal interactions. In a 2025 longitudinal study of trauma-exposed adults, improvements in executive control functions correlated with reduced atrophy in the cornu ammonis 1 region of the hippocampus, a stress-vulnerable area, measured via MRI volumetry over 6-12 months post-event.^[83]^[84] This plasticity is mediated by activity-dependent gene expression, including brain-derived neurotrophic factor (BDNF) upregulation, which promotes synaptogenesis and counters glucocorticoid-induced dendritic retraction.^[85] Animal models corroborate these findings, showing that enriched environments post-stress enhance neural progenitor proliferation in the dentate gyrus, analogous to human resilience-promoting interventions like cognitive behavioral therapy.^[86] Behavioral plasticity complements neural changes, with resilient individuals exhibiting flexible coping strategies that leverage prior learning to buffer future stressors. Meta-analyses of prospective cohort studies report that higher baseline cognitive reserve—built through education and bilingualism—predicts better post-traumatic adjustment, with effect sizes of Cohen's d = 0.4-0.6, attributed to reserve-induced plasticity in frontoparietal networks.^[81] Early life adversity (ELA) studies further reveal that resilient trajectories involve epigenetic adaptations, such as methylation changes in stress-response genes (e.g., NR3C1), enabling adaptive plasticity rather than maladaptive rigidity; for instance, a 2025 review synthesized data from over 20 human cohorts showing that 20-30% of ELA-exposed individuals achieve resilience via such mechanisms.^[87]^[80] Interventions targeting plasticity, such as aerobic exercise, induce dose-dependent increases in hippocampal neurogenesis, with randomized trials demonstrating 2-5% volume gains after 6 months of moderate-intensity training (150 minutes/week), correlating with improved resilience scores on scales like the Connor-Davidson Resilience Scale.^[88] However, plasticity's efficacy diminishes with repeated or prolonged stress, as evidenced by cumulative glucocorticoid exposure exceeding 10-15 mg/day prednisone equivalents leading to impaired long-term potentiation in vitro models, underscoring resilience as a dynamic process rather than an immutable trait.^[86]^[89] Overall, these findings highlight plasticity's causal role in resilience, with therapeutic potential in preventing psychopathology through targeted enhancement of adaptive neural remodeling.^[82]

Critiques and Philosophical Perspectives

Destructive Plasticity Concept

Destructive plasticity, a concept introduced by philosopher Catherine Malabou, denotes the brain's inherent capacity for sudden, irreversible transformations that rupture established neuronal forms and identities, often triggered by trauma, accidents, or lesions such as strokes. Malabou argues this facet of plasticity contrasts with its more commonly emphasized regenerative or adaptive dimensions, emphasizing instead an "explosive" process where synaptic and structural integrity is destroyed, leading to the emergence of alien or vacated subjectivities devoid of prior continuity. In her 2012 work The Ontology of the Accident, she draws on neurological cases of brain injury to illustrate how such events suspend psychic life, fostering split identities or emotional detachment, as seen in patients exhibiting profound apathy post-trauma. This ontological dimension posits destructive plasticity as integral to human subjectivity, where form-giving yields to form-breaking, incorporating death-like processes into life's continuity—such as neuronal pruning escalated to catastrophic levels.^[90] Malabou critiques overly optimistic neuroscientific narratives of plasticity as mere flexibility, insisting that true plasticity encompasses destruction as a generative force for alterity, exemplified in literary analogies like Kafka's Metamorphosis, where inexplicable transformation mirrors traumatic neural reconfiguration.^[91] Philosophically, it challenges deterministic views of the self, proposing that accidents reveal plasticity's dual power to sculpt and demolish, potentially informing understandings of conditions like depression or post-traumatic disorders where emotional life is "vacated."^[92] Neuroscience evaluations of the term, however, highlight its interpretive rather than empirical framing; while maladaptive synaptic changes occur in pathologies—such as long-term potentiation strengthening pain circuits in chronic conditions—plasticity mechanisms remain value-neutral tools for adaptation, not inherently destructive.^[93] A 2024 analysis contends that labeling such processes "destructive" anthropomorphizes neutral rewiring, as evidenced by studies showing post-injury reorganization can yield functional recovery despite initial form loss, urging terminological precision to avoid implying teleological negativity.^[93] Malabou's concept, rooted in Hegelian dialectics and selective neuroimaging interpretations, thus serves more as a philosophical heuristic for trauma's existential rupture than a strictly neurobiological descriptor, with limited direct experimental validation beyond observed maladaptive outcomes in epilepsy or addiction models.^[93]^[94]

Debunking Overhyped Claims

Claims that neuroplasticity enables boundless rewiring of the brain to fully restore lost functions, such as sight or mobility after severe injury, or to achieve superhuman cognitive enhancements through casual interventions, pervade popular books like Norman Doidge's The Brain's Way of Healing.^[95] These narratives suggest near-infinite adaptability, with examples including visualization techniques alleviating chronic pain or exercise mitigating Parkinson's symptoms, but such outcomes demand extreme, repetitive effort and remain anecdotal or limited in scope, not generalizable cures.^[95] Empirical reviews indicate that full sensory or motor restoration is rare, often involving compensatory mechanisms rather than original circuit revival, as evidenced by cases where neurofeedback aids locked-in syndrome communication but fails to reverse paralysis.^[95] Brain training applications and programs, such as those from Michael Merzenich's BrainHQ or Lumosity, hype neuroplasticity as a tool for age-defying cognitive rejuvenation via gamified exercises, promising transferable gains in memory, attention, and IQ.^[96] Yet, controlled trials reveal minimal evidence of broad skill transfer beyond practiced tasks, with meta-analyses showing effects confined to near-transfer without impacting real-world functioning or delaying decline.^[96] This overreach exemplifies neuroessentialism, where neural mechanisms are invoked to justify unsubstantiated psychological claims, ignoring environmental and behavioral factors in learning.^[97] Research on cortical adaptation challenges assertions of dramatic reorganization; for instance, visual cortex responses in congenitally blind individuals activate latent pathways present from development, not newly forged networks, as demonstrated in functional imaging studies of cross-modal plasticity.^[98]^[99] Adult plasticity exhibits further constraints, with experiments like those rewiring ocular dominance in animals showing reliance on early developmental windows and intensive training, yielding adjustments within existing architecture rather than wholesale repurposing.^[98] Marketing of vagus nerve stimulators or nootropics as plasticity "hacks" similarly lacks causal validation, often conflating habit formation with structural neural change.^[97] True plasticity operates via specific processes like heterosynaptic strengthening, but its therapeutic limits—evident in partial stroke recoveries—underscore that hype eclipses the need for targeted, evidence-based interventions over panacea promises.^[96]

References

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Plasticity - an overview | ScienceDirect Topics
Plasticity is defined as the property of materials that allows them to undergo permanent deformation under applied stress without fracturing.
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Phenotypic Plasticity: From Theory and Genetics to Current and ...
Phenotypic plasticity is defined as the property of organisms to produce distinct phenotypes in response to environmental variation.
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Neuroplasticity - StatPearls - NCBI Bookshelf - NIH
Neuroplasticity, also known as neural plasticity or brain plasticity, is a process that involves adaptive structural and functional changes to the brain.
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12.6: Elasticity and Plasticity - Physics LibreTexts
Sep 12, 2022 · For stresses beyond the elastic limit, a material exhibits plastic behavior. This means the material deforms irreversibly and does not return to ...
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Phenotypic plasticity in development and evolution: facts and concepts
Feb 27, 2010 · Phenotypic plasticity is the ability of individual genotypes to produce different phenotypes when exposed to different environmental conditions.
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Phenotypic plasticity made simple, but not too simple - PMC - NIH
Phenotypic plasticity is environment-dependent trait expression, described by the reaction norm, which is the set of phenotypes a genotype expresses in ...
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What Is Neural Plasticity? - PubMed
Neural plasticity refers to the capacity of the nervous system to modify itself, functionally and structurally, in response to experience and injury.
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The Impact of Studying Brain Plasticity - Frontiers
Neural plasticity, also known as neuroplasticity or brain plasticity, can be defined as the ability of the nervous system to change its activity in response ...
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MIT scientists discover fundamental rule of brain plasticity
Jun 22, 2018 · Our brains are famously flexible, or “plastic,” because neurons can do new things by forging new or stronger connections with other neurons.
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Phenotypic Plasticity - an overview | ScienceDirect Topics
Phenotypic plasticity is the ability of an organism to change in response to stimuli or inputs from the environment. Synonyms are phenotypic responsiveness, ...
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[PDF] Yield strength – the stress beyond which a material becomes plastic
Yield strength – the stress beyond which a material becomes plastic; yielding is both useful (forming, absorbing energy) and dangerous. • This chapter focuses ...
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Yielding (Chapter 2) - Fundamentals of Engineering Plasticity
Jun 5, 2013 · Of concern in plasticity theory is the yield strength, which is the level of stress that causes appreciable plastic deformation.
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Slip in Single Crystals (all content) - DoITPoMS
When a single crystal is deformed under a tensile stress, it is observed that plastic deformation occurs by slip on well-defined parallel crystal planes.
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[PDF] Characteristics of dislocations • Slip systems • Slip in single crystals
Dislocations & plastic deformation. • Cubic & hexagonal metals - plastic deformation by plastic shear or slip where one plane of atoms slides over adjacent ...
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The Plastic Deformation Mechanisms of hcp Single Crystals ... - NIH
Feb 4, 2021 · In hcp metals, the most popular plastic deformation mechanisms are slip and twinning. In general, slip is always along the lattice close ...<|separator|>
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Mechanisms of Plasticity (all content) - DoITPoMS
From the viewpoint of plastic deformation, the most important type of dislocation intersection is the intersection of two screw dislocations (Figure 7). The ...
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Crystal Plasticity Finite Element Method - Dierk Raabe
Crystal Plasticity Finite Element (CPFE) models use variational methods to solve equilibrium and displacement compatibility, using a dyadic velocity gradient ...
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Multiscale crystal plasticity finite element model for investigating the ...
A multiscale crystal plasticity finite element model, which combines molecular dynamics with crystal plasticity theory, is proposed.
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Advancements in and Applications of Crystal Plasticity Modelling of ...
ICME provides improved understanding of the mechanics of the material, through which two main aspects of a material's lifecycle are addressed, namely the ...
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Finite difference based stress integration algorithm for crystal ...
Jan 4, 2024 · In this study, we present a Finite Difference Method (FDM)-based stress integration algorithm for Crystal Plasticity Finite Element Method (CPFEM).
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[PDF] Multiscale Modelling of Plasticity - OSTI.gov
Aug 22, 2019 · Given the rapid progress in computational and experimental techniques, a new generation of multiscale models of crystal plasticity is expected ...
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[PDF] Multiscale modeling of the plasticity in an aluminum single crystal
This paper describes a numerical, hierarchical multiscale modeling methodology involving two distinct bridges over three different.
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Multiscale modeling of plastic deformation of molybdenum and ...
In this paper, we develop a link between the atomic-level modeling of the glide of 1/2 < 111 > screw dislocations at 0 K and the thermally activated motion ...Missing: metals | Show results with:metals
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Discovering plasticity models without stress data - Nature
Apr 28, 2022 · Our objective here is to discover fully general and evolving plastic yield surfaces, which characterize the material behavior of three- ...
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Deep learning predicts path-dependent plasticity - PNAS
Dec 16, 2019 · We show that material plasticity can be precisely and efficiently predicted by deep-learning methods.Abstract · Theoretical Approach · Results
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A machine learning based plasticity model using proper orthogonal ...
The machine learning based plasticity model is developed by using of a novel method called Proper Orthogonal Decomposition Feed forward Neural Network (PODFNN).
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Machine Learning Reinforced Crystal Plasticity Modeling Under ...
This Paper addresses a two-step computational approach to building a robust modeling environment for the titanium–aluminum alloy, Ti-7Al, ...
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Rethinking phenotypic plasticity and its consequences for ... - Nature
Oct 8, 2014 · Plasticity is oftentimes defined as the ability of a single genotype to exhibit a range of different phenotypes in response to variation in the ...
[29]
Benefits of phenotypic plasticity for population growth in varying ...
Nov 26, 2018 · Phenotypic plasticity refers to the capacity of the same organisms to exhibit different characteristics under varied environmental conditions.
[30]
Phenotypic plasticity in development and evolution: facts and concepts
Phenotypic plasticity can be defined as 'the ability of individual genotypes to produce different phenotypes when exposed to different environmental conditions' ...
[31]
Constraints on the evolution of phenotypic plasticity: limits and costs ...
Feb 18, 2015 · Phenotypic plasticity has long been recognized as a key strategy enabling organisms to respond to varying environments both adaptively and non- ...
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Strong phenotypic plasticity limits potential for evolutionary ... - Nature
Mar 8, 2018 · Phenotypic plasticity, the expression of multiple phenotypes from one genome, is a widespread adaptation to short-term environmental ...
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Phenotypic plasticity promotes species coexistence - Nature
Aug 4, 2022 · Phenotypic plasticity allows genetically identical individuals to express different phenotypes in response to changes in abiotic or biotic ...
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New frontiers in phenotypic plasticity and evolution | Heredity - Nature
Sep 16, 2015 · In particular, plasticity is thought to have a major role in evolution by allowing survival in novel environments ('Baldwin Effect' sensu ...
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The role of phenotypic plasticity on population differentiation - Nature
Jul 26, 2017 · Overall, plasticity decouples genetic from phenotypic differences between populations, and blurs the correlation between phenotypic divergence and local ...<|separator|>
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https://www.cell.com/trends/ecology-evolution/fulltext/S0169-5347(22)00216-6
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Phenotypic Plasticity and Integration in Response to Flooded ... - NIH
Genetic differentiation and phenotypic plasticity at the single‐trait and multivariate levels were investigated in 47 accessions of the weedy plant Arabidopsis ...
[38]
Characterization, costs, cues and future perspectives of phenotypic ...
There are numerous examples of adaptive plastic responses, including reduced root secondary growth in common bean as a response to phosphorus stress (Strock et ...
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[PDF] Phenotypic plasticity for plant development, function and life history
For example, the proportions of staminate and hermaphroditic flowers in an andromonoecious Solanum were shown to depend on plant resource status, confirming a ...
[40]
[PDF] Phenotypic Plasticity and Interactions Among Plants
Perhaps the best examples are those of plasticity in stem elongation, clonal architecture, and photosynthetic chemistry. High densities of neighbors often have ...
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Sensory Ecology of Predator-Induced Phenotypic Plasticity - PMC
Jan 18, 2019 · Daphnia shows plastic responses by adapting its morphology, behavior, and physiology, increasing organism, and population fitness. This stabilizes community ...
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Predator-induced phenotypic plasticity within- and across-generations
Jan 7, 2015 · Notably, many species of water fleas (Daphnia) respond to the presence of predators by producing morphological defences (head and tail spines) ...
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Endocrine regulation of predator-induced phenotypic plasticity - PMC
Oct 5, 2014 · We investigate the physiological regulation of phenotypic plasticity induced by another organism, specifically predator-induced phenotypic plasticity.
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Color Change, Phenotypic Plasticity, and Camouflage - Frontiers
May 17, 2016 · For example, aside from crabs, chameleon prawns (Hippolyte varians) change to a blue-gray color, and animals from various other taxa undergo ...Abstract · Which Animals Change Color... · How Does Color Change and...
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The neuroplastic brain: current breakthroughs and emerging frontiers
Jul 1, 2025 · This overview article examines synaptic plasticity, structural remodeling, neurogenesis, and functional reorganization, highlighting both adaptive (beneficial) ...
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Dynamic Brains and the Changing Rules of Neuroplasticity - Frontiers
Oct 3, 2017 · In this article, we will provide several lines of evidence indicating that mechanisms of neuroplasticity are extremely variable across individuals and ...Missing: empirical | Show results with:empirical
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Maintaining a Dynamic Brain: A Review of Empirical Findings ...
May 14, 2024 · Abstract. Brain plasticity, also termed neuroplasticity, refers to the brain's life-long ability to reorganize itself in response to.
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Neuroplasticity: a century-old idea championed by Adolf Meyer - PMC
Dec 9, 2019 · In 1902, Adolf Meyer (seated, with friends in a family photo) called the nervous system the “apparatus of biological plasticity”and placed the ...Missing: key | Show results with:key
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A Systematic Review Focusing on Molecular Imaging Using PET
Aug 20, 2025 · This systematic review provides a comprehensive overview of evidence for neuroplasticity in healthy and diseased human brains, focusing on PET ...
[50]
The neuroplastic brain: current breakthroughs and emerging frontiers
Jul 1, 2025 · This overview provides an in-depth exploration of neuroplasticity's mechanisms, examines emerging therapeutic approaches including ...
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[PDF] The Role and Importance of Neuroplasticity in ... - JournalAgent
Sep 1, 2024 · 24 It is proposed that physi- cal exercise may promote brain plasticity by increasing the release of Brain-Derived Neurotrophic Factor (BDNF), ...
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Exploring the Role of Neuroplasticity in Development, Aging, and ...
2.1. Structural Neuroplasticity. Structural neuroplasticity refers to physical changes to neural circuits, including the growth of new dendritic spines, axonal ...
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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.Introduction · Experience-Dependent Spine... · Molecular Mechanisms of...
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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.
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Activity-Dependent Synaptogenesis in the Adult Mammalian Cortex
Most inhibitory synapses occur on dendrites (dark blue), with a small proportion on spines (light blue). Following whisker stimulation, there is a shift in the ...
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Imaging functional neuroplasticity in human white matter tracts - PMC
Nov 23, 2021 · Magnetic resonance imaging (MRI) studies are sensitive to biological mechanisms of neuroplasticity in white matter (WM).
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Neuroplasticity after Traumatic Brain Injury - NCBI - NIH
Weeks after injury, new synaptic markers and axonal sprouting are upregulated, allowing for remodeling and cortical changes for recovery. Chronic changes have ...
[58]
Experience, Cortical Remapping, and Recovery in Brain Disease
This means that remapping in the motor cortex could result from changes in the brain stem and spinal cord, areas that are more difficult to access ...
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Reorganization and plastic changes of the human brain associated ...
This mini review will attempt to take a narrow snapshot of imaging findings demonstrating functional and structural plasticity that mediate skill learning and ...
[60]
Imaging Brain Plasticity: Conceptual and Methodological Issues
The neural plasticity associated with learning and development is increasingly being studied using functional neuroimaging methods such as positron emission ...
[61]
Structural LTP: from synaptogenesis to regulated synapse ...
Dendritic spines are tiny protrusions that stud the surface of dendrites and host most of the excitatory synapses throughout the brain. The importance of ...
[62]
Neuroplasticity of Brain Networks Through Exercise: A Narrative ...
Studies suggest that exercise can induce structural changes in different brain regions and modulate functional connectivity between brain areas, thereby ...
[63]
Evidence for Neuroplasticity in the Human Brain in Health and ...
Jul 18, 2025 · Neuroplasticity is the ability of the brain to show persistent structural and/or functional modifications in response to external changes.
[64]
Recovery after brain injury: mechanisms and principles - Frontiers
This paper will review the current theoretical models and empirical evidence for functional plasticity in the cortical motor system.
[65]
Critical periods of brain development - PubMed
Brain plasticity is maximal at specific time windows during early development known as critical periods (CPs), during which sensory experience is necessary.
[66]
Rejuvenation of plasticity in the brain: opening the critical period
These observations triggered the idea of “critical periods,” which are optimal periods of development when brain circuits acquire and store information [1–5].
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Neural plasticity in the ageing brain | Nature Reviews Neuroscience
Jan 1, 2006 · This review focuses on age-related changes in the neurobiology of the hippocampus and the prefrontal cortex (PFC) and how altered synaptic ...Key Points · Main · Glossary
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Age-related changes in responsiveness to non-invasive brain stimulation neuroplasticity paradigms: A systematic review with meta-analysis
- **Number of Studies**: 39 studies, encompassing 40 experiments, were reviewed.
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Stanford Medicine study hints at ways to generate new neurons in ...
Oct 2, 2024 · The researchers' finding suggests the possibility of designing pharmaceutical or genetic therapies to turn on new neuron production in old or injured brains.<|separator|>
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CRISPR–Cas9 screens reveal regulators of ageing in neural stem ...
Oct 2, 2024 · Ageing impairs the ability of neural stem cells (NSCs) to transition from quiescence to proliferation in the adult mammalian brain.
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Emerging mechanisms of psilocybin-induced neuroplasticity
Sep 15, 2025 · Psilocin might interact with intracellular 5-HT2ARs, possibly mediating psilocin's sustained neuroplastic effects through location-biased ...
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Methylone promotes neurite outgrowth and has long-lasting effects ...
Aug 23, 2025 · Alterations in structural neuroplasticity are a well-studied mechanism that may underlie both the pathophysiology and treatment of PTSD.
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Modulating neuroplasticity for chronic pain relief: noninvasive ...
Mar 3, 2025 · This review aims to critically examine the mechanisms of maladaptive neuroplasticity in chronic neuropathic pain and evaluate the efficacy of noninvasive ...Missing: breakthroughs | Show results with:breakthroughs
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Epigenetic regulation of brain development, plasticity, and response ...
Aug 6, 2025 · For example, breakthrough work from more than twenty years ago discovered that depolarization of neurons in vitro induces DNA demethylation at ...
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Brain training game boosts chemical linked to memory and attention ...
Oct 19, 2025 · A new study finds that a cognitive training program may boost production of a brain chemical that plays a role in memory and attention.<|control11|><|separator|>
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Developmental plasticity: Bridging research in evolution and human ...
Feb 5, 2018 · The shaping of later life traits by early life environments, known as 'developmental plasticity', has been well-documented in humans and non-human animals.
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Genomics of Developmental Plasticity in Animals - Frontiers
This review focuses on intra-generational developmental plasticity in animals, including an overview of its reciprocal effects on evolution.
[78]
Neuroimaging of plasticity mechanisms in the human brain - Nature
Aug 13, 2022 · Critical periods are windows of programmed neurodevelopmental plasticity wherein external inputs exert large and lasting impacts on the organization of neural ...<|control11|><|separator|>
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The role of developmental plasticity in evolutionary innovation
Jun 15, 2011 · Longstanding theory suggests that developmental plasticity, the ability of an individual to modify its development in response to environmental ...Introduction · Developmental plasticity and... · Developmental genetic basis...
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Biological and Psychological Perspectives of Resilience - NIH
Whether resilience should be defined as a trait, process or outcome is frequently debated in human resilience studies. ... Psychological resilience: a review and ...
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Neurocognitive Mechanism of Human Resilience: A Conceptual ...
... psychological resilience may help us better understand the causes and ... Chronic stress and brain plasticity: Mechanisms underlying adaptive and ...
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Human Brain Resilience: A Call to Action - PMC - PubMed Central
Network reorganization and the mechanisms of neuroplasticity ... Measures of adult psychological resilience following early-life adversity: how congruent are ...
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Plasticity of human resilience mechanisms - PubMed
Jan 10, 2025 · Human resilience to trauma is characterized by the plasticity of memory control circuits, which interacts with hippocampal neuroplasticity.
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Plasticity of human resilience mechanisms - PMC - PubMed Central
Jan 8, 2025 · Human resilience to trauma is characterized by the plasticity of memory control circuits, which interacts with hippocampal neuroplasticity.
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https://www.uclahealth.org/sites/default/files/documents/mcewen-resilience.pdf
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Neurobiological Mechanisms of Stress Resilience and Implications ...
... human resilience are still in their infancy. The development of animal ... Molecular aging of the brain, neuroplasticity, and vulnerability to depression and ...
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[PDF] A Comprehensive Overview of Stress, Resilience, and ...
Mar 26, 2025 · The aim of this review was to synthesize recent advances in the understanding of the neuroplasticity mechanisms underlying resilience to ELS. We.
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Lifestyle Modulators of Neuroplasticity: How Physical Activity, Mental ...
... brain plasticity during aging. The Journals of Gerontology. Series A ... Psychological resilience in young and older adults. International Journal of ...
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[PDF] Resilience: An Update - National Center for PTSD
Here we review important extant evidence in animal models and humans. Although the precise mechanisms of plasticity are still not fully understood, moderate to ...<|separator|>
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Catherine Malabou's “Destructive Plasticity” - Ifilnova
Oct 7, 2024 · “Destructive plasticity” thus concerns the paramount role of death in life processes: in order to give and take form, subjectivity needs to “ ...
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Ontology Of The Accident By Catherine Malabou - Society & Space
May 27, 2013 · Gregor waking up as a giant insect without cause or understanding is an example of destructive plasticity; an inexplicable transformation and ...
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The Old Wounded: Destructive Plasticity and Intergenerational Trauma
May 22, 2018 · ... destruction of form. The plasticity at stake here is thus destructive plasticity. It is important to recognize here that, according to ...
[93]
Rethinking plasticity: Analysing the concept of “destructive plasticity ...
Aug 2, 2024 · Consequently, the term “destructive” may be scientifically inadequate, as it implies that this plasticity inherently drives towards destruction.Abstract · PLASTICITY: A KEY... · EMERGENCE OF A... · POSSIBILITIES FOR...
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Maladaptive myelination promotes generalized epilepsy progression
May 2, 2022 · This includes the generalized genetic epilepsies and the often devastating developmental and epileptic encephalopathy Lennox–Gastaut syndrome.Missing: destructive | Show results with:destructive
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Let's Not Overstretch Neuroplasticity | by Maia Szalavitz | proto.life
Sep 20, 2018 · Many of those authors argue that the possibilities of plasticity are nearly infinite—that it can restore sight, hearing, and movement to people ...
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Neural plasticity: don't fall for the hype | The British Academy
Jun 16, 2017 · Neural plasticity is certainly a ubiquitous phenomenon but is no panacea to all our problems. Don't fall for the neural plasticity hype! 1.
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Thinking Beyond the Brain: Why Neuroplasticity is Overhyped
If you see “neuroplasticity” being used to sell a supplement or a brain training app, you can be almost certain that it's being overhyped for marketing purposes ...
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The Brain Isn't as Adaptable as Some Neuroscientists Claim
Nov 21, 2023 · The answer, our research suggests, lies not in the brain's ability to undergo dramatic reorganization but in the power of training and learning.
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https://doi.org/10.7554/eLife.84716