Fact-checked by Grok 2 weeks ago

Neural pathway

A neural pathway, also known as a neural tract or circuit, is a series of interconnected neurons and their axons that transmit electrochemical signals from one region of the to another, enabling the communication and processing of sensory, motor, and cognitive information. These pathways form the foundational architecture of the and , consisting of afferent neurons that carry signals toward the , efferent neurons that convey signals away from it, and that integrate and modulate local processing within the circuit. Synaptic connections between these neurons occur in the —a dense network of dendrites, axon terminals, and glial processes—allowing for precise information relay through excitatory or inhibitory . Neural pathways are broadly classified into sensory (ascending) pathways, which relay information from peripheral receptors to the for ; motor (descending) pathways, which direct voluntary and involuntary movements from the to muscles; and association pathways, which integrate signals within the for higher functions like learning and . In the spinal cord, these pathways manifest as tracts—bundles of myelinated s grouped by function, such as the for fine motor control or the for pain and temperature sensation. Pathways develop during embryogenesis through guided growth and formation, influenced by genetic cues and environmental factors, and exhibit throughout life, adapting via strengthening or weakening of s in response to experience or injury. The functionality of neural pathways underpins essential physiological processes, including reflexes like the myotatic , where sensory afferents trigger rapid muscle responses through direct excitatory and inhibitory circuits. Disruptions in these pathways, such as those caused by , , or neurodegenerative diseases, can lead to deficits in , , or , highlighting their critical role in and disease. Advances in , including imaging techniques like diffusion tensor imaging, have enabled detailed mapping of these pathways, revealing their intricate organization and potential for therapeutic intervention.

Introduction and Fundamentals

Definition and Characteristics

A neural pathway is a series of interconnected neurons that transmit electrochemical signals from one region of the nervous system, such as a sensory receptor or brain area, to another, facilitating the processing of information and generation of responses. These pathways form the foundational routes for communication within the central and peripheral nervous systems, consisting of axons bundled into tracts in the brain and spinal cord. Key characteristics of neural pathways include their potential for unidirectional or bidirectional signal flow, depending on the circuit; involvement of synapses that allow for modulation of signals through excitatory or inhibitory interactions; and specificity in , which can be direct (with minimal intervening neurons) or indirect (involving multiple relays for integration). Pathways often incorporate and re-entrant loops, supported by glial cells and myelinated axons that enhance conduction velocity. They play a central role in forming larger neural circuits that underpin sensory , , and cognitive functions. Basic types of neural pathways are distinguished by the number of synapses involved: monosynaptic pathways feature a single between sensory and motor neurons, as seen in the where muscle spindles directly activate alpha motor neurons to contract the muscle and counteract stretch. In contrast, polysynaptic pathways involve multiple and for more complex integration, such as in pain transmission via the , where nociceptive signals from peripheral receptors relay through several spinal before ascending to the . Neural pathways exhibit evolutionary conservation across vertebrates, with core sensory and motor circuits, including those for risk avoidance and reward seeking, present in ancestral forms and maintained through tetrapods due to their essential role in behaviors. Variations in complexity arise, from simpler reflex-based pathways in to elaborate, multi-layered networks in mammals that support advanced processing.

Historical Context and Naming Conventions

The concept of neural pathways emerged in the late , rooted in advancements in histological techniques that allowed visualization of individual neurons. Camillo Golgi's development of the staining method in the 1870s enabled selective labeling of nerve cells, revealing their intricate structures for the first time. Building on this, refined the technique in the 1880s and 1890s, producing detailed drawings that demonstrated neurons as discrete, independent units rather than a continuous network. This work culminated in Cajal's neuron doctrine, articulated around 1890, which posited that the nervous system consists of interconnected but separate cellular elements forming pathways for signal transmission. Cajal's findings, supported by his studies of the and other regions, shifted understanding from reticular theories to a modular view of neural organization. In the , key milestones further elucidated specific neural pathways through experimental approaches. studies, pioneered in the but expanded in the early 1900s, involved inducing or observing brain damage to map functional deficits, leading to the identification of major tracts like the corticospinal pathway. A landmark advancement came in the 1950s and 1960s with David Hubel and Torsten Wiesel's electrophysiological recordings in cats and monkeys, which revealed hierarchical processing in visual pathways from the to the . Their discovery of orientation-selective cells in the demonstrated how pathways integrate sensory information, earning them the in Physiology or Medicine in 1981. Naming conventions for neural pathways evolved from early descriptive terms to more systematic . Initially, pathways were labeled based on eponyms or , but by the mid-20th century, standards shifted toward origin and destination, as seen in the (from cortex to ). Functional descriptors emerged for specialized circuits, such as the reward pathway (mesolimbic system), while regional names like the denoted limbic interconnections. This progression toward standardization was formalized by the Federative Committee on Anatomical Terminology, which published Terminologia Anatomica in 1998, providing Latin-based terms for neuroanatomical structures including pathways to ensure global consistency. Technological influences refined pathway mapping beyond traditional . Post-1990s developments in (MRI), particularly diffusion tensor imaging (DTI) introduced in the late 1990s, enabled non-invasive to trace bundles , improving accuracy over lesion-based methods. This shift, building on MRI's clinical adoption in the 1980s, allowed three-dimensional reconstruction of pathways like the optic radiations, transforming historical concepts into dynamic, verifiable models. Subsequent efforts, such as the launched in 2010 and AI-assisted analyses in the 2020s, have further advanced high-resolution mapping of neural pathways in humans and model organisms.

Anatomical and Physiological Basis

Structure and Components

Neural pathways are primarily composed of axons, which serve as the main conduits for transmitting electrical impulses between neurons. These axons are often insulated by sheaths, fatty layers produced by glial cells that enhance signal speed and efficiency by enabling . Synapses form the critical junctions where axons connect to dendrites or cell bodies of other neurons, facilitating the release of neurotransmitters to propagate signals across the pathway. Supporting glial cells, particularly in the , play a key role in myelination and maintaining axonal integrity. At the organizational level, neural pathways incorporate tracts, which are bundles of myelinated axons forming the that carry signals over long distances within the . Nuclei consist of clusters of neuronal cell bodies in the gray matter, acting as stations or hubs along these pathways. Broader neural circuits emerge from interconnected pathways, integrating multiple tracts and nuclei to enable coordinated information flow. Neural pathways exhibit a hierarchical structure, beginning with peripheral nerves that interface with the body and progressing to tracts, relays, and ultimately cortical projections in the . This organization includes ascending (afferent) pathways that convey sensory information toward higher centers and descending (efferent) pathways that transmit commands from the to effectors. Pathway architecture demonstrates variability through , where a single influences multiple downstream neurons, and , where inputs from many neurons integrate onto one. For instance, the , a major interhemispheric pathway, spans an average length of approximately 7.8 cm in humans, illustrating the scale of these long-range connections.

Mechanisms of Signal Transmission

Signal transmission in neural pathways occurs primarily through the generation and propagation of action potentials along axons, followed by chemical communication at synapses. The action potential is an all-or-nothing electrical event, meaning it either occurs at full amplitude or not at all once a threshold is reached, triggered by the opening of voltage-gated sodium channels that allow Na⁺ influx, depolarizing the from its of approximately -70 mV. This is followed by the opening of voltage-gated channels, enabling K⁺ efflux to repolarize the . The resting arises mainly from the unequal distribution of ions across the neuronal , approximated by the for :
V_K = \frac{RT}{F} \ln \left( \frac{[K^+]_o}{[K^+]_i} \right),
where R is the , T is temperature, F is Faraday's constant, and [K^+]_o and [K^+]_i are extracellular and intracellular concentrations, respectively; adjustments for sodium permeability yield the overall resting potential via the Goldman-Hodgkin-Katz equation.
At synapses, action potentials arriving at the presynaptic terminal trigger calcium influx, leading to the fusion of synaptic vesicles with the membrane and of neurotransmitters into the synaptic cleft. Excitatory neurotransmitters like glutamate bind to postsynaptic receptors, opening channels that cause and generate excitatory postsynaptic potentials (EPSPs), while inhibitory neurotransmitters such as hyperpolarize the membrane via chloride influx, producing inhibitory postsynaptic potentials (IPSPs). These potentials summate through temporal summation, where repeated inputs from the same presynaptic add over time, or spatial summation, where inputs from multiple presynaptic s combine simultaneously to influence whether the postsynaptic fires an action potential. In myelinated axons, which are insulated by myelin sheaths formed by oligodendrocytes or Schwann cells, signal propagation occurs via saltatory conduction, where action potentials "jump" between nodes of Ranvier, greatly increasing speed to 70–120 m/s in humans compared to 0.5–10 m/s in unmyelinated fibers undergoing continuous conduction. This efficiency allows rapid transmission over long distances in neural pathways. Neural pathways integrate signals through , where multiple presynaptic onto a single postsynaptic to amplify or refine inputs, and , where one presynaptic influences many postsynaptic to broadcast signals across networks. A foundational principle of such integration is the Hebbian rule, stating that "neurons that fire together wire together," describing how correlated activity strengthens synaptic connections to facilitate coordinated pathway function.

Classification of Neural Pathways

Sensory Neural Pathways

Sensory neural pathways, also known as ascending pathways, transmit information from peripheral sensory receptors to central structures for processing. These pathways generally originate from specialized receptors such as photoreceptors in the or mechanoreceptors in the skin, relaying signals through a series of neurons to the and then to the , with the exception of the . The major subtypes include somatosensory, visual, auditory, and olfactory pathways, each adapted to specific modalities of sensory input. The somatosensory pathway conveys tactile, proprioceptive, pain, and temperature sensations from the body. It comprises two primary tracts: the dorsal column-medial lemniscus pathway, which handles fine touch, vibration, and proprioception with high spatial resolution, and the anterolateral (spinothalamic) pathway, which processes crude touch, pain, and temperature with less precise localization. In the dorsal column-medial lemniscus system, primary afferents ascend ipsilaterally in the spinal cord's posterior columns to synapse in the medullary gracile and cuneate nuclei; secondary fibers then decussate and form the medial lemniscus, projecting to the ventral posterolateral (VPL) nucleus of the thalamus and onward to the primary somatosensory cortex in the postcentral gyrus. The spinothalamic tract involves primary afferents synapsing in the spinal cord's dorsal horn, with secondary fibers decussating immediately and ascending contralaterally to the VPL thalamus and somatosensory cortex. These pathways exhibit somatotopic organization, mapping the body surface onto the cortex in a distorted representation known as the sensory homunculus, where larger cortical areas correspond to densely innervated regions like the hands and face. The visual pathway begins at photoreceptors in the , where and cells process light signals to form the . Axons from retinal ganglion cells travel to the , where approximately 50% decussate—fibers from the nasal cross to the contralateral side—ensuring that each optic tract carries information from the contralateral . The optic tracts terminate in the (LGN) of the , which relays segregated magnocellular (motion-sensitive) and parvocellular (color- and detail-sensitive) inputs via the optic radiations to the primary () in the occipital lobe's . This pathway maintains retinotopic organization, preserving spatial relationships from the to the . In the auditory pathway, sound vibrations activate hair cells in the , which synapse with neurons whose axons form the (cranial nerve VIII) to reach the ipsilateral cochlear nuclei in the . From there, projections ascend to the binaural for sound localization cues like interaural time differences, then via the to the in the for integration of acoustic features. The pathway continues to the (MGN) of the , which relays tonotopically organized information—preserving frequency maps—to the primary in the temporal lobe's Heschl's . The olfactory pathway uniquely bypasses the , providing direct sensory access to cortical and limbic structures. Olfactory sensory neurons in the nasal , each expressing a single odorant receptor, project axons through the to glomeruli in the , where they with mitral and tufted cells. These second-order neurons send distributed projections to the , including the , anterior olfactory nucleus, and , as well as to the cortical and for emotional and memory associations. This direct route facilitates rapid odor processing and contrasts with the thalamic relay in other sensory systems.

Motor Neural Pathways

Motor neural pathways encompass descending tracts that transmit signals from higher brain centers, such as the and , to the and ultimately to skeletal muscles, enabling voluntary and reflexive . These pathways are broadly classified into pyramidal and extrapyramidal systems. The pyramidal system involves direct projections from the to lower motor neurons, facilitating precise, voluntary movements, while the comprises indirect pathways via nuclei and , which modulate posture, tone, and automatic movements. The pyramidal tract, also known as the , originates primarily from the (), with contributions from premotor areas, somatosensory cortex, and . Fibers descend through the , , cerebral peduncles, and , forming compact bundles called the medullary pyramids. At the caudal medulla, approximately 85-90% of these fibers decussate at the pyramidal decussation, forming the that travels contralaterally in the 's lateral funiculus to synapse with anterior horn cells in the , enabling skilled, fractionated voluntary movements of the limbs and trunk. The remaining 10-15% form the anterior corticospinal tract, which descends ipsilaterally and crosses at spinal levels for midline control. Lesions in this tract lead to contralateral weakness, particularly affecting fine motor skills. Extrapyramidal pathways provide supplementary motor control through multisynaptic routes originating from brainstem structures. The rubrospinal tract arises from the red nucleus in the midbrain tegmentum, decussates at the ventral tegmental level, and descends contralaterally in the lateral funiculus to influence flexor muscle tone and facilitate distal limb movements, such as those of the hands and fingers, in coordination with the corticospinal tract. The vestibulospinal tract originates from vestibular nuclei in the medulla and pons, with the lateral component projecting ipsilaterally to extensor motor neurons in the spinal cord's ventral horn (laminae VII-VIII), maintaining posture and balance by exciting extensors and inhibiting flexors during equilibrium adjustments. The reticulospinal tract, from pontine and medullary reticular formation, descends bilaterally via anterior and lateral funiculi to modulate axial and proximal muscle tone, supporting locomotion and postural reflexes by facilitating extensor activity. Cerebellar influences on motor pathways occur indirectly, without direct efferents to the , primarily through the dentate in the lateral cerebellar nuclei. The dentate receives inputs from the cerebellar lateral hemisphere (cerebrocerebellum) and projects contralaterally via the to the ventrolateral thalamic , which relays to the for fine-tuning movement coordination, timing, and accuracy. This pathway enables and error correction, such as in skilled tasks requiring precise muscle synergies. Alpha motor neurons in the spinal cord's anterior horn serve as the final common pathway for all descending motor signals, integrating inputs from pyramidal and extrapyramidal tracts to directly innervate fibers via neuromuscular junctions, as originally described by Sir Charles Sherrington. These neurons form motor units that execute contractions for both voluntary and reflexive actions. , a spinal reflex mechanism, ensures coordinated movement by inhibiting antagonist muscles when agonists contract; for instance, activation of flexor motor neurons via Ia afferent feedback from muscle spindles disynaptically suppresses extensor motor neurons through inhibitory , preventing co-contraction and facilitating smooth joint motion.

Association Neural Pathways

Association neural pathways, also referred to as intracerebral or commissural connections, facilitate the integration of sensory, motor, and cognitive information within the , supporting higher-order functions such as learning, , , and executive control. Unlike sensory and motor pathways that primarily connect the periphery to the or vice versa, association pathways link different regions of the and subcortical structures, including the (e.g., connections between the and for ) and circuits (e.g., cortico-striatal loops for reward processing and formation). These pathways enable cross-hemispheric communication via commissures like the and are essential for complex behaviors, with disruptions linked to disorders like and .

Key Neural Pathways in the Brain

Basal Ganglia Pathways

The comprise a group of subcortical nuclei involved in , including the (composed of the and ), the (divided into external and internal segments, GPe and GPi), the subthalamic nucleus (STN), and the (with pars compacta and pars reticulata, SNc and SNr). These structures form interconnected loops that modulate cortical output via the , with the serving as the primary input site from the and the GPi and SNr as the main output nuclei projecting inhibitory signals to the . The direct pathway originates in the striatum's medium spiny neurons expressing , which provide inhibitory projections directly to the GPi and SNr; this inhibition reduces the tonic suppression of thalamocortical neurons by the output nuclei, thereby facilitating and promoting selected actions. The circuit flows from to , then to GPi/SNr, , and back to , closing a loop that enhances desired motor programs through of the ventral anterior and ventrolateral thalamic nuclei. In contrast, the indirect pathway involves striatal neurons with D2 that inhibit the GPe; this leads to of the STN, which then excites the GPi and SNr via projections, increasing inhibition of the and suppressing competing or unwanted movements to refine action selection. from the SNc modulates these pathways by exciting direct pathway neurons and inhibiting indirect ones, balancing facilitation and suppression. A third route, the hyperdirect pathway, provides rapid cortical input directly to the STN from motor and premotor areas, bypassing the ; the STN then excites GPi/SNr to quickly inhibit thalamic activity and halt ongoing or inappropriate movements. This pathway enables fast phasic responses, such as stopping, and integrates with the and indirect routes to dynamically select actions by promoting some while suppressing others. The overall balance of these pathways ensures precise through re-entrant cortico-basal ganglia-thalamocortical loops, with disruptions like depletion in overactivating the indirect pathway and underactivating the direct, leading to bradykinesia and rigidity.

are a set of neural circuits in the where serves as the primary , originating primarily from nuclei such as the pars compacta (SNc) and the (VTA). These pathways modulate various functions including , reward processing, , and endocrine regulation, rather than providing direct excitatory or inhibitory drive; instead, acts as a neuromodulator influencing the efficacy of other synaptic transmissions. The arises from neurons in the SNc and projects to the dorsal ( and ), playing a crucial role in and the formation of stimulus-response habits. Degeneration of this pathway, involving the loss of up to 80-90% of neurons in the SNc, underlies the motor symptoms of , such as bradykinesia and rigidity. The originates in the VTA and innervates the and other limbic structures, facilitating motivation, reward anticipation, and ; disruptions here contribute to , as seen with , which blocks the () to prevent and prolong synaptic availability. The also stems from the VTA but targets the , supporting like , , and . Finally, the extends from the arcuate nucleus of the , which contains a distinct group of neurons, to the and pituitary, regulating hormone release, particularly inhibiting secretion via 's action as a prolactin-inhibiting factor. Dopamine is synthesized in these neurons from the L-tyrosine, with (TH) catalyzing the rate-limiting step to form , which is then decarboxylated to by . Upon release, binds to G-protein-coupled receptors divided into D1-like (D1 and D5; Gs-coupled, excitatory via increased and enhanced neuronal excitability) and D2-like (D2, D3, D4; Gi-coupled, inhibitory via decreased and reduced excitability) families, allowing fine-tuned modulation of target circuits. In the , facilitates habit formation by strengthening stimulus-response associations in the dorsal , as evidenced by studies showing that lesions or depletion impair the shift from goal-directed to habitual behavior. The drives motivation and addiction vulnerability; for instance, phasic bursts in the encode reward prediction errors, and chronic exposure enhances this signaling to promote compulsive drug-seeking. Post-1990s () imaging, using tracers like [11C]-raclopride for D2 receptors or [18F]-DOPA for synthesis, has mapped density, revealing high concentrations in the (e.g., nigrostriatal terminals) and lower but functionally critical levels in limbic and cortical targets, aiding diagnosis of pathway-specific deficits in disorders like Parkinson's.

Functional Roles and Dynamics

Role in Behavior and Cognition

Neural pathways play a pivotal role in integrating sensory, emotional, and motor signals to orchestrate complex behaviors, particularly through reward systems that motivate goal-directed actions. The , originating from dopaminergic neurons in the and projecting to the , is essential for encoding reward anticipation and reinforcing behaviors that lead to positive outcomes, thereby driving individuals toward adaptive, goal-oriented pursuits such as or social interaction. In parallel, motor neural pathways, including the corticospinal and cortico-rubral tracts, translate these motivational signals into precise physical execution, enabling the coordinated muscle activation required for voluntary movements and behavioral responses. In cognitive domains, prefrontal neural pathways facilitate higher-order processes like and by maintaining transient representations of relevant information across delays. Pathways connecting the to parietal regions support the active manipulation of mental representations, allowing for and flexible responses to environmental demands. Complementing this, the —comprising interconnected pathways between the medial prefrontal cortex, posterior cingulate, and —activates during introspective states, such as or self-referential thinking, to integrate past experiences with future simulations. At the circuit level, specific neural loops exemplify these contributions; for instance, the hippocampal-entorhinal cortex loop, involving reciprocal projections between CA1/CA3 regions of the and layers II/III of the , underpins spatial navigation through place cells that fire selectively in distinct environmental locations, enabling path integration and memory-guided exploration. Similarly, the amygdala-prefrontal pathway, with bidirectional connections from the basolateral amygdala to the medial , modulates by associating neutral stimuli with aversive outcomes, thereby shaping avoidance behaviors critical for survival. Inter-pathway interactions further enhance via loops that dynamically couple sensory inputs, motor outputs, and limbic ; for example, ascending sensory pathways from the relay environmental cues to limbic structures like the , which in turn influence descending motor commands through prefrontal gating, allowing real-time adjustments in response to changing contexts. These loops ensure that behaviors remain flexible and contextually appropriate, balancing immediate reactions with long-term goals. A key distinction in behavioral control arises from the interplay between habit formation and goal-directed actions, as delineated in 2010s frameworks. Model-free learning, reliant on cached value estimates along striatal pathways, supports habitual behaviors that are efficient but inflexible, whereas model-based learning, involving prefrontal-hippocampal circuits that simulate outcomes, enables deliberate, goal-directed choices by incorporating explicit of action-reward contingencies. This dichotomy highlights how neural pathways differentially contribute to automatic versus volitional control, with dopaminergic signaling in the mesolimbic system briefly modulating the balance toward reinforcement of either mode.

Plasticity and Modulation

Neural pathways exhibit remarkable , enabling adaptive changes in connectivity and strength that underpin learning, , and recovery from injury. , a core mechanism, involves (LTP) and long-term depression (), which strengthen or weaken synaptic efficacy, respectively, primarily through activation. LTP is induced by high-frequency that depolarizes the postsynaptic , relieving the magnesium block on s and allowing calcium influx, which triggers signaling cascades like CaMKII activation to enhance insertion and synaptic potentiation. Conversely, LTD arises from low-frequency , producing modest calcium rises that activate phosphatases such as , leading to endocytosis and synaptic weakening. These bidirectional changes follow principles akin to the Hebbian rule, where synaptic weight updates are proportional to correlated pre- and postsynaptic activity, formalized as \Delta w = \eta \cdot x \cdot y with \Delta w as the weight change, \eta the learning rate, x presynaptic activity, and y postsynaptic activity. Structural plasticity complements synaptic modifications by altering neural architecture, including axon sprouting and dendritic spine remodeling. In response to injury or learning, axons can sprout new branches to form compensatory connections, while dendritic spines—small protrusions housing most excitatory synapses—undergo morphological changes such as growth, shrinkage, or turnover to support strengthened pathways. Studies from the 1990s demonstrated that exposure to enriched environments, featuring novel objects and social interaction, increases dendritic spine density and synaptic contacts in the hippocampus and cortex of rodents, enhancing overall circuit complexity. Modulation of neural pathways occurs through neuromodulators that fine-tune activity without directly transmitting signals, often by altering synaptic gain or excitability. Serotonin, released from , modulates pathway strength by binding to receptors that influence potassium channels, thereby adjusting neuronal firing thresholds and promoting adaptive responses to environmental cues. Similarly, acetylcholine from projections enhances signal-to-noise ratios in cortical pathways by increasing presynaptic release probability and postsynaptic responsiveness via muscarinic and nicotinic receptors. These effects are experience-dependent, as seen in critical periods of visual pathway development, where deprivation during early postnatal stages leads to enduring shifts in columns due to heightened mediated by inhibition. Pathway-specific adaptations highlight plasticity's targeted nature, such as following , where undamaged regions expand representations to restore lost functions like through perilesional sprouting and transcallosal projections. Metaplasticity, the plasticity of itself, further regulates these changes by altering the threshold for inducing LTP or based on prior activity history, preventing saturation and enabling stable long-term modifications. At the molecular level, (BDNF) expression drives many processes by promoting stabilization and dendritic growth via TrkB receptor signaling, with activity-induced transcription essential for LTP maintenance. operates across diverse timescales, from short-term facilitation lasting milliseconds via presynaptic calcium dynamics to long-term structural reorganizations spanning years, allowing pathways to adapt to both rapid sensory inputs and chronic experiential demands.

Clinical Significance

Disorders Involving Neural Pathways

Disorders involving neural pathways encompass a range of neurological and psychiatric conditions resulting from structural damage, degeneration, or functional dysregulation in specific tracts and circuits. These disruptions impair , leading to characteristic symptoms that reflect the affected pathway's role in , , or . Diagnosis often relies on advanced techniques like MRI , which emerged in the post-2000s era to visualize integrity and connectivity abnormalities non-invasively. Motor disorders frequently arise from lesions or degeneration in descending pathways, such as the or circuits. In , progressive loss of dopaminergic neurons in the disrupts pathways, resulting in depletion that manifests as bradykinesia, rigidity, and ; this condition affects approximately 1% of individuals over age 60 worldwide. Genetic factors, including mutations in the gene, contribute to 1-5% of sporadic cases and 5-13% of familial Parkinson's, exacerbating pathway vulnerability. involves striatal degeneration, particularly of medium spiny neurons in the , leading to —involuntary, jerky movements—due to impaired indirect pathway function and excitotoxic damage from protein. Stroke-induced hemiplegia often stems from ischemic damage to the in the or , causing contralateral by interrupting voluntary motor signals from the . Sensory disorders typically involve ascending pathways, where demyelination or axonal injury disrupts somatosensory transmission. features focal demyelination of tracts, including dorsal column-medial lemniscus pathways, resulting in such as tingling or numbness due to slowed or blocked action potentials along affected fibers. , often from or toxins, damages ascending sensory nerves in peripheral pathways, leading to numbness and loss of as disrupted fibers fail to relay tactile and pain signals to the and . Cognitive and psychiatric disorders highlight dysregulation in limbic and prefrontal pathways. is associated with hypoactivity, where reduced signaling from the to the contributes to cognitive deficits and negative symptoms, while mesolimbic hyperactivity underlies positive symptoms like delusions. involves hypersensitivity, particularly in the , where repeated drug exposure sensitizes release and strengthens reward cues, driving compulsive behavior through neuroplastic changes. features atrophy of hippocampal-entorhinal pathways, with neuronal loss and tau pathology severing connections critical for , resulting in progressive impairment.

Therapeutic Interventions

Therapeutic interventions for neural pathway dysfunctions encompass pharmacological, surgical, neuromodulatory, rehabilitative, and emerging approaches aimed at restoring circuit integrity and function. Pharmacological treatments often target imbalances in specific pathways. , a dopamine precursor, replenishes depleted levels in the of patients, alleviating motor symptoms through conversion to via dopa decarboxylase. Clinical trials demonstrate reduces Unified Parkinson's Disease Rating Scale (UPDRS) motor scores by 50-70% in early-stage disease, though long-term use can induce dyskinesias. Selective serotonin reuptake inhibitors (SSRIs), such as , inhibit serotonin reuptake via the SLC6A4 transporter, enhancing activity in serotonergic pathways implicated in mood regulation for . This mechanism increases synaptic serotonin, with chronic administration desensitizing 5-HT1A autoreceptors to promote downstream signaling. Surgical and neuromodulatory techniques provide targeted circuit modulation. (DBS) of the subthalamic nucleus, FDA-approved in 2002 for advanced , delivers high-frequency electrical pulses to normalize aberrant oscillations, yielding 40-60% improvements in UPDRS motor scores and reducing levodopa requirements. In February 2025, the FDA approved adaptive DBS systems, such as Medtronic's BrainSense, which dynamically adjust stimulation based on neural biomarkers to further optimize treatment outcomes in Parkinson's patients. , developed post-2005, employs light-activated opsins (e.g., ) to precisely excite or inhibit neural pathways in preclinical models of disorders like and , offering millisecond control unavailable with electrical methods. Rehabilitative strategies harness activity-dependent plasticity to reorganize impaired pathways. Constraint-induced movement therapy (CIMT) restricts unaffected limbs post-, forcing use of the paretic side to drive cortical remapping in motor pathways, with randomized trials showing 20-30% gains in upper extremity function via the Wolf Motor Function Test. Repetitive (rTMS) non-invasively induces cortical excitability changes, enhancing ipsilesional motor pathway connectivity and improving outcomes in rehabilitation. Emerging therapies focus on genetic and cellular repair of pathways. (AAV)-based , such as approved by the FDA in 2019 for , delivers functional genes to pathways via systemic infusion, achieving survival rates over 90% in infants without permanent ventilation. implants, including mesenchymal stem cells, promote remyelination in demyelinated pathways of , with phase I/II trials reporting reduced lesion volumes and stabilized disability scores on the (EDSS); as of 2025, ongoing phase III trials continue to evaluate long-term efficacy. Manipulating neural pathways raises ethical concerns, including risks to from unintended circuit alterations and challenges in obtaining for irreversible interventions like or , necessitating rigorous oversight to balance therapeutic benefits against potential autonomy erosion.

References

  1. [1]
    Neural Pathway - an overview | ScienceDirect Topics
    Neural pathways consist of interconnected neurons that transmit information throughout the nervous system. · They can be classified as motor pathways, sensory ...Structural and Functional... · Neural Pathways and... · Neural Pathways in...
  2. [2]
    Neural Circuits - Neuroscience - NCBI Bookshelf - NIH
    The synaptic connections that define a circuit are typically made in a dense tangle of dendrites, axons terminals, and glial cell processes that together ...
  3. [3]
    Neural pathways and spinal cord tracts: Anatomy | Kenhub
    Neural pathways are groups of nerve fibers which carry information between the various parts of the CNS. Neural pathways that connect the CNS and spinal cord ...
  4. [4]
    Introduction to Neurons and Neuronal Networks | Section 1, Intro ...
    Dendrites are the region where one neuron receives connections from other neurons. The cell body or soma contains the nucleus and the other organelles necessary ...
  5. [5]
    Stretch Reflex - an overview | ScienceDirect Topics
    16.1 is also known as the monosynaptic stretch reflex because this reflex is mediated by a single (“mono”) synaptic relay in the central nervous system.
  6. [6]
    Physiology, Withdrawal Response - StatPearls - NCBI Bookshelf - NIH
    The withdrawal reflex is polysynaptic, meaning that, in addition to the sensory and motor neurons, this response utilizes interneurons, which pass signals ...
  7. [7]
    Evolution of vertebrate survival circuits - ScienceDirect.com
    As discussed in the following sections, the neural circuits mediating these behaviours are evolutionarily conserved (at least in tetrapod vertebrates), and give ...
  8. [8]
    Golgi, Cajal and the Neuron Doctrine - PubMed
    Camillo Golgi and Santiago Ramon y Cajal shared the Nobel Prize in 1906 for their work on the histology of the nerve cell, but both held diametrically opposed ...
  9. [9]
    Cajal, the neuronal theory and the idea of brain plasticity - Frontiers
    Cajal discovered and named dendritic spines when he was studying the cerebellum of birds using Golgi's method in 1888 (Cajal, 1888a,b). In 1890 he also ...
  10. [10]
    Neurology through history: The advent of the neuron doctrine
    Dec 5, 2023 · Using Golgi's staining method, Cajal painstakingly illustrated that the nervous system was composed of individual units—neurons--that were ...
  11. [11]
    Lesion studies in contemporary neuroscience - PMC - PubMed Central
    Studies on the effects of permanent lesions provide vital data about brain function that are distinct from those of reversible manipulations.
  12. [12]
    The Nobel Prize in Physiology or Medicine 1981 - Press release
    Through the discoveries of Hubel and Wiesel we now know that behind the origin of the visual perception in the brain there is a considerably more complicated ...Missing: pathways | Show results with:pathways
  13. [13]
    David Hubel and Torsten Wiesel - PubMed
    Jul 26, 2012 · Hubel and Wiesel's work provided fundamental insight into information processing in the visual system and laid the foundation for the field of visual ...
  14. [14]
    Neuroanatomy - an overview | ScienceDirect Topics
    Neuroanatomy is defined as the foundational language of neuroscience, encompassing a hierarchical nomenclature system that provides location references ...Missing: destination | Show results with:destination
  15. [15]
    Terminologia anatomica: new terminology for the new anatomist
    FCAT has worked for 9 years and published Terminologia Anatomica (TA) in 1998. FCAT's aim has been to democratize the terminology and make it the ...Missing: neural pathways
  16. [16]
    Diffusion-Tensor MR Imaging and Tractography - RSNA Journals
    Diffusion MR tractography offers an overall view of brain anatomy, including the degree of connectivity between different regions of the brain.
  17. [17]
    Tractography for Surgical Neuro-Oncology Planning: Towards a ...
    Dec 12, 2018 · Introduction of magnetic resonance imaging (MRI) in the 1980s permitted detailed, noninvasive visualization of neural parenchyma in both normal ...Missing: post- | Show results with:post-
  18. [18]
    Nerve Tissue - SEER Training Modules - National Cancer Institute
    Many axons are surrounded by a segmented, white, fatty substance called myelin or the myelin sheath. Myelinated fibers make up the white matter in the CNS ...
  19. [19]
    Neuronal Types - Developmental Biology - NCBI Bookshelf - NIH
    The oligodendrocyte wraps itself around the developing axon. It then produces a specialized cell membrane called a myelin sheath. In the peripheral nervous ...
  20. [20]
    Histology at SIU, Neurons and Support Cells
    Synapses are points of contact between nerve cells (usually between axon terminals and dendrites), where signals are transmitted from one cell to another. ( ...
  21. [21]
    Cells of the Nervous System: Glia – Introduction to Neuroscience
    The main function of the oligodendrocytes is to add a layer of myelin around the axons of nearby neurons in the central nervous system.
  22. [22]
    Anatomy of the Spinal Cord (Section 2, Chapter 3) Neuroscience ...
    The spinal cord white matter contains ascending and descending tracts. Ascending tracts (Figure 3.8). The nerve fibers comprise the ascending tract emerge ...
  23. [23]
    Lab 2 Spinal Cord Gray Matter
    Columns of neuron cell bodies, when transected, appear as clusters of neuron cell body profiles within gray matter. The cell body clusters are called nuclei.
  24. [24]
    Anatomy, Central Nervous System - StatPearls - NCBI Bookshelf - NIH
    Oct 10, 2022 · The nervous system is divided into the central nervous system (CNS) and the peripheral nervous system. The CNS includes the brain and spinal cord.
  25. [25]
    Corpus Callosum and Its Connections: A Fiber Dissection Study
    May 24, 2021 · Results: The mean length of the corpus callosum from the rostrum to the splenium was 7.8 cm. The fibers of the corpus callosum were classified ...
  26. [26]
    Physiology, Action Potential - StatPearls - NCBI Bookshelf - NIH
    In neurons, the rapid rise in potential, depolarization, is an all-or-nothing event that is initiated by the opening of sodium ion channels within the plasma ...
  27. [27]
    Chapter 2. Ionic Mechanisms of Action Potentials
    Sodium conductance decreases, the membrane potential begins to repolarize, and the Na+ channels that are open and not yet inactivated are deactivated and close.
  28. [28]
    The Forces that Create Membrane Potentials - Neuroscience - NCBI
    For a simple hypothetical system with only one permeant ion species, the Nernst equation allows the electrical potential across the membrane at equilibrium to ...
  29. [29]
    Synaptic Transmission
    The presynaptic membrane and vesicle now forms a continuous membrane, so that the neurotransmitter is released into the synaptic cleft. This process is called ...
  30. [30]
    Amino Acid Neurotransmitters (Section 1, Chapter 13) Neuroscience ...
    These are the processes of temporal and spatial summation. ... neuron and this glutamate can immediately be pumped into vesicles for subsequent release.
  31. [31]
    Ch. 6: Synaptic Transmission in the Central Nervous System
    The processes by which the multiple EPSPs from presynaptic neurons summate over space and time are called temporal and spatial summation. Figure 6.3. Temporal ...
  32. [32]
    Myelin: A Specialized Membrane for Cell Communication - Nature
    For example, conduction velocity in the most thoroughly myelinated axons (12–20 μm in diameter) is 70–120 m/s (race car speed), although other factors such as ...
  33. [33]
    Increased Conduction Velocity as a Result of Myelination - NCBI - NIH
    Unmyelinated axon conduction velocities range from about 0.5 to 10 m/s, myelinated axons can conduct at velocities up to 150 m/s.
  34. [34]
    Hebbian Theory - an overview | ScienceDirect Topics
    20 The Hebbian hypothesis, “Neurons that fire together, wire together,” provides a theoretical basis for linking plasticity during sensory system development ...Introduction to Hebbian Theory... · Hebbian Plasticity in Neural...
  35. [35]
    Ascending Sensory Pathways – Introductory Neuroscience Review ...
    Except for the olfactory system, all ascending sensory pathways include a synapse in the thalamus. Some sensory systems like vision and somatosensation are ...
  36. [36]
    Somatosensory Pathways (Section 2, Chapter 4) Neuroscience Online
    Sensory pathways consist of the chain of neurons, from receptor organ to cerebral cortex, that are responsible for the perception of sensations. Somatosensory ...Missing: review | Show results with:review
  37. [37]
    Chapter 15: Visual Processing: Cortical Pathways
    Visual processing starts in the retina, then goes to the lateral geniculate nucleus (LGN) of the thalamus, and finally to the striate cortex (V1) in the ...
  38. [38]
    Auditory System: Central Processing – Introduction to Neuroscience
    For the auditory system, following the activation of hair cells within the cochlea, sound information is transmitted to brain structures including the thalamus ...
  39. [39]
    Neuroanatomy, Pyramidal Tract - StatPearls - NCBI Bookshelf - NIH
    The pyramidal tract originates from the cerebral cortex, and it divides into two main tracts: the corticospinal tract and the corticobulbar tract.
  40. [40]
    Neuroanatomy, Extrapyramidal System - StatPearls - NCBI Bookshelf
    Prus postulated that, apart from pyramidal tracts, there must be alternative pathways, called the "extrapyramidal tracts," that "delivered epileptic activity" ...Introduction · Structure and Function · Blood Supply and Lymphatics
  41. [41]
    Neuroanatomy, Corticospinal Cord Tract - StatPearls - NCBI Bookshelf
    Aug 14, 2023 · The corticospinal tract, AKA, the pyramidal tract, is the major neuronal pathway providing voluntary motor function.
  42. [42]
    Cerebellum (Section 3, Chapter 5) Neuroscience Online
    The dentate nucleus is the largest of the cerebellar nuclei, located lateral to the interposed nuclei. It receives input from the lateral hemisphere and from ...
  43. [43]
    Motor Units and Muscle Receptors (Section 3, Chapter 1 ...
    The famous physiologist Sir Charles Sherrington referred to these motor neurons as the “final common pathway” in motor processing. ... With low rates of activity ...
  44. [44]
    Abnormal reciprocal inhibition between antagonist muscles in ...
    Disynaptic Ia reciprocal inhibition acts, at the spinal level, by actively inhibiting antagonist motor neurons and reducing the inhibition of agonist motor ...
  45. [45]
    The functional anatomy of basal ganglia disorders - ScienceDirect.com
    Basal ganglia disorders are a heterogeneous group of clinical syndromes with a common anatomic locus within the basal ganglia.
  46. [46]
    Functional significance of the cortico–subthalamo–pallidal ...
    The cortico–subthalamo–pallidal 'hyperdirect' pathway conveys powerful excitatory effects from the motor-related cortical areas to the globus pallidus, ...
  47. [47]
    Dopamine: Functions, Signaling, and Association with Neurological ...
    Together with the four main pathways, nigrostriatal, mesolimbic, mesocortical, and tuberoinfundibular, there is another diencephalic dopaminergic cluster in ...
  48. [48]
    Dopamine: The Neuromodulator of Long-Term Synaptic Plasticity ...
    Dopamine (DA) is a key neurotransmitter involved in multiple physiological functions including motor control, modulation of affective and emotional states, ...
  49. [49]
    Loss of dopaminergic nigrostriatal neurons accounts for ... - PubMed
    Parkinson's disease (PD) involves the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) that is thought to cause the ...
  50. [50]
    Neurobiologic Processes in Drug Reward and Addiction - PMC
    The DAT is responsible for reabsorbing synaptic DA back into the presynaptic neuron, and occupancy of the DAT by cocaine prevents DA re-uptake.
  51. [51]
    Tyrosine hydroxylase and regulation of dopamine synthesis - PubMed
    Apr 1, 2011 · Tyrosine hydroxylase is the rate-limiting enzyme of catecholamine biosynthesis; it uses tetrahydrobiopterin and molecular oxygen to convert ...
  52. [52]
    Biochemistry, Dopamine Receptors - StatPearls - NCBI Bookshelf
    There are five types of dopamine receptors, which include D1, D2, D3, D4, and D5. Each receptor has a different function and is found in different locations.Introduction · Fundamentals · Function · Pathophysiology
  53. [53]
    Lesion to the Nigrostriatal Dopamine System Disrupts Stimulus ...
    Mar 16, 2005 · The aim of the present experiments was to study the role of the nigrostriatal dopaminergic pathway in instrumental habit formation. For this ...
  54. [54]
    Positron emission tomography imaging of dopamine D2 receptors ...
    Positron emission tomography (PET) is an in vivo imaging technique which is capable of providing measures of receptor density in the living human brain. To date ...
  55. [55]
    Behavioral Functions of the Mesolimbic Dopaminergic System
    The ML-DA system is central to motivated behaviors, reward, and cognitive processes, activating a "SEEKING" state for life-supporting stimuli and influencing ...
  56. [56]
    The role of motor cortex in motor sequence execution depends ... - NIH
    Lesioning motor cortex showed that it is necessary for flexible cue-driven motor sequences but dispensable for single automatic behaviors trained in isolation.
  57. [57]
    The Role of Prefrontal Cortex in Working Memory: A Mini Review - NIH
    A widely held view of prefrontal cortex (PFC) function is that it encodes task relevant information in working memory (Goldman-Rakic, 1987; Miller and Cohen, ...
  58. [58]
    20 years of the default mode network: a review and synthesis - PMC
    The author reviews the role of the default mode network (DMN) in human cognition, proposing that the DMN integrates and broadcasts memory, language, and ...Missing: pathways | Show results with:pathways
  59. [59]
    Spatial and memory circuits in the medial entorhinal cortex - PMC
    Entorhinal grid cells provide inputs to the hippocampus, and their firing patterns shift relative to each other across different environments. Although this ...
  60. [60]
    The amygdala and medial prefrontal cortex: partners in the fear circuit
    In this review, we discuss the neuronal circuits within, and between the mPFC and amygdala and their roles in fear conditioning and extinction. The amygdala.Missing: paper | Show results with:paper
  61. [61]
  62. [62]
    The neurochemical substrates of habitual and goal-directed control
    Mar 3, 2020 · Lesion to the nigrostriatal dopamine system disrupts stimulus-response habit formation. J. Neurosci. 25, 2771–2780 (2005). Article CAS ...
  63. [63]
    NMDA Receptor-Dependent Long-Term Potentiation and Long ...
    Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-d-aspartate (NMDA)-type glutamate receptors.Missing: seminal | Show results with:seminal
  64. [64]
    Mathematical formulations of Hebbian learning - PubMed
    Hebbian learning uses correlation-based formulations, with presynaptic activity described by firing rate or spike arrival, and postsynaptic state by membrane ...
  65. [65]
    Structural plasticity of dendritic spines - PMC - PubMed Central - NIH
    These studies strongly support the view that the structure and contents of a dendritic spine can undergo long-term modifications during synaptic plasticity.Missing: enriched environments
  66. [66]
    Effects of environmental enrichment on gene expression in the brain
    In conclusion, environmental enrichment affects the expression levels of a number of genes involved in neuronal structure, synaptic signaling, and plasticity.<|control11|><|separator|>
  67. [67]
    Neuromodulation of Attention - Neuron - ScienceDirect.com
    Feb 21, 2018 · Neuromodulators most strongly implicated in high-level cognitive functions are acetylcholine (ACh), dopamine (DA), noradrenaline (NA), and ...
  68. [68]
    Acetylcholine as a neuromodulator: cholinergic signaling shapes ...
    We propose that the role of ACh as a neuromodulator in the brain is to increase neurotransmitter release in response to other inputs, to promote burst firing ...
  69. [69]
    Development and Plasticity of the Primary Visual Cortex - PMC - NIH
    Hubel and Wiesel began the modern study of development and plasticity of primary visual cortex (V1), discovering response properties of cortical neurons.
  70. [70]
    Cortical reorganization after stroke: how much and how functional?
    Jun 17, 2013 · Here, we review key advances over the past two decades that have shed light on the neural mechanisms enabling recovery of motor function after stroke.
  71. [71]
    Metaplasticity: tuning synapses and networks for plasticity - Nature
    the plasticity of synaptic plasticity — and considers its importance for nervous ...
  72. [72]
    BDNF and synaptic plasticity, cognitive function, and dysfunction
    BDNF plays a critical role in hippocampal long-term potentiation (LTP), a long-term enhancement of synaptic efficacy thought to underlie learning and memory.
  73. [73]
    Time scales of memory, learning, and plasticity
    Nov 18, 2012 · In this prospect we review these mechanisms with respect to their time scale and propose relations between mechanisms in learning and memory and ...<|control11|><|separator|>
  74. [74]
    The Usefulness of Diffusion Tensor Tractography in Diagnosing ...
    Mar 25, 2021 · DTT allows a quantitative analysis of healthy and pathological nerves, myelin sheaths, and muscles and enables the assessment of neural tract ...
  75. [75]
    Current Clinical Applications of Diffusion-Tensor Imaging in ...
    Feb 28, 2018 · Advanced diffusion MRI fiber tracking in neurosurgical and neurodegenerative disorders and neuroanatomical studies: a review. Biochim ...
  76. [76]
    Role of dopamine in the pathophysiology of Parkinson's disease
    Sep 18, 2023 · A pathological feature of Parkinson's disease (PD) is the progressive loss of dopaminergic neurons and decreased dopamine (DA) content in the substantia nigra ...
  77. [77]
    Parkinson's Disease: What It Is, Causes, Symptoms & Treatment
    Experts estimate that it affects at least 1% of people over age 60 worldwide. How does this condition affect my body? Parkinson's disease causes a specific ...Cleveland Clinic Parkinson's... · Essential Tremor · Corticobasal Degeneration
  78. [78]
    The Role of LRRK2 in Neurodegeneration of Parkinson Disease
    Mutations in LRRK2 are account for 5–13% of familial PD and 1–5% of sporadic PD [20]. Seven of the reported missense LRRK2 mutations have been identified as ...
  79. [79]
    The mechanism of degeneration of striatal neuronal subtypes in ...
    The pattern of neurodegeneration in Huntington's disease (HD) is very characteristic of regional locations as well as that of neuronal types in striatum.
  80. [80]
    The role of corticospinal and extrapyramidal pathways in motor ... - NIH
    Anisotropy of descending motor pathways has repeatedly been linked to the severity of motor impairment following stroke-related damage to the corticospinal ...
  81. [81]
    Multiple sclerosis | Nature Reviews Disease Primers
    Nov 8, 2018 · Sensory symptoms include paresthesia (commonly described as numbness, tingling ... Damage to sensory nerve tracts in MS leads to chronic ...
  82. [82]
    Peripheral Neuropathy | National Institute of Neurological Disorders ...
    Aug 7, 2024 · People with the disorder often notice a patch of skin in the area that is sensitive to touch and sometimes painful, numb, or tingling. Most ...
  83. [83]
    The Role of Dopamine in Schizophrenia from a Neurobiological and ...
    May 19, 2014 · The positive symptoms of schizophrenia include hallucinations and delusions as a result of increased subcortical release of dopamine, which ...
  84. [84]
    Neuroplasticity in the mesolimbic dopamine system and cocaine ...
    Jan 29, 2009 · These neuroadaptations have been hypothesized to cause hypersensitivity to cocaine-associated cues (;), impulsive decision making (;) and ...Role Of Bdnf · Bdnf: Cocaine... · Vta: Psychomotor...<|separator|>
  85. [85]
    Hippocampus and its involvement in Alzheimer's disease: a review
    Feb 1, 2022 · Lack of sirtuin (SIRT) expression in the hippocampal neurons will impair cognitive function, including recent memory and spatial learning.
  86. [86]
    Levodopa (L-Dopa) - StatPearls - NCBI Bookshelf - NIH
    Apr 17, 2023 · Levodopa is the precursor to dopamine. Most commonly, clinicians use levodopa as a dopamine replacement agent for the treatment of Parkinson disease.
  87. [87]
    Depletion of dopamine in Parkinson's disease and relevant ...
    This review tries to explain the different possible mechanisms behind the depletion of dopamine in PD patients such as alpha-synuclein abnormalities, ...
  88. [88]
    Selective Serotonin Reuptake Inhibitors - StatPearls - NCBI Bookshelf
    May 1, 2023 · As the name suggests, SSRIs exert action by inhibiting the reuptake of serotonin, thereby increasing serotonin activity.Continuing Education Activity · Indications · Mechanism of Action · Adverse Effects
  89. [89]
    Selective Serotonin Reuptake Inhibitors (SSRI) Pathway - PMC
    The molecular target for SSRI is SCL6A4, resulting in an inhibition of 5-HT reuptake in the presynapse from the synaptic cleft. The five SSRI fluoxetine, ...
  90. [90]
    A history of deep brain stimulation: Technological innovation and the ...
    In 2002, deep brain stimulation (DBS) for the treatment of Parkinson's disease (PD) was granted approval by the US Food and Drug Administration (FDA). Since ...
  91. [91]
    Comparison of Globus Pallidus Interna and Subthalamic Nucleus in ...
    The UPDRS III is used universally as a scale to measure the motor improvement after DBS and is assessed in varying combinations, with medication off and on and ...<|separator|>
  92. [92]
    The Roles of Optogenetics and Technology in Neurobiology: A Review
    Apr 19, 2022 · Using optogenetics to induce the differentiation of neural progenitor cells, the researchers were able to treat stroke in mice (Yu et al., 2019 ...
  93. [93]
    Optogenetics and its application in neural degeneration and ...
    This short review presents representative work in optogenetics in disease models such as spinal cord injury, multiple sclerosis, epilepsy, Alzheimer's disease ...
  94. [94]
    The neural basis of constraint-induced movement therapy - PubMed
    Summary: CIMT is the first well defined poststroke motor rehabilitation to have identified changes in brain function and structure that accompany gains in motor ...
  95. [95]
    Constraint-Induced Movement Therapy Results in Increased Motor ...
    Constraint-induced movement therapy (CIMT) has produced promising results among subjects with limited upper extremity motor function after stroke.
  96. [96]
    Repetitive Transcranial Magnetic Stimulation - StatPearls - NCBI - NIH
    Mar 6, 2023 · Repetitive transcranial magnetic stimulation (rTMS) is a safe and non-invasive treatment technique used to treat various psychiatric and neurological disorders.
  97. [97]
    Evidence of Neuroplastic Changes after Transcranial Magnetic ...
    For TMS, neuroplasticity is commonly indexed by the change in cortical excitability before and after application of a course of repetitive TMS, which is ...
  98. [98]
    Recombinant Adeno-Associated Virus Serotype 9 Gene Therapy in ...
    In May 2019, FDA approved the first onasemnogene abeparvovec, the first gene replacement therapy for the treatment of SMA patients with <2 years of age with bi ...
  99. [99]
    [PDF] May 24, 2019 Summary Basis for Regulatory Action - ZOLGENSMA
    May 24, 2019 · The ongoing Phase 3 trial and the completed Phase 1 trial form the basis of the review team's recommendation for regular approval of ZOLGENSMA ...
  100. [100]
    Stem cell therapy for multiple sclerosis - PMC - PubMed Central - NIH
    Stem cell therapy has shown promising results and has attracted attention as an alternative therapeutic option for people with MS.
  101. [101]
    Mesenchymal stem cell therapy: A review of clinical trials for multiple ...
    Specialized stem cells, known as mesenchymal stem cells (MSCs), seem to be the candidate therapy to get rid of MS.
  102. [102]
    Neuromodulation and memory: exploring ethical ramifications in ...
    Dec 21, 2023 · Ethical concerns include identity harm, disrupting self-narratives, altering moral and emotional responsiveness, and potential moral ...
  103. [103]
    Taking Optogenetics into the Human Brain - PubMed Central - NIH
    This review looks at the reasons why researchers are exploring the use of optogenetics within the brain. It then explores the challenges facing scientists, ...