Journal September 19, 2026 6 min read

How does neuroplasticity work?

Neuroplasticity is the nervous system's capacity to reorganize its structure and function in response to experience, injury, or therapeutic intervention. This page examines the molecular and cellular mechanisms under inv

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Neuroplasticity is the nervous system's capacity to reorganize its structure and function in response to experience, injury, or therapeutic intervention. It encompasses synaptic plasticity (changes in strength and number of connections), structural plasticity (axonal sprouting, dendritic remodeling, and in some regions adult neurogenesis), and network-level reorganization. The term is sometimes used interchangeably with 'neural plasticity' or 'brain plasticity'. No single molecular formula or identifier applies because neuroplasticity is a process, not a compound; the evidence below concerns specific modulators and interventions studied in relation to it.

The work centres on several interacting pathways and receptor families, including neurotrophin signalling (notably brain-derived neurotrophic factor, BDNF, acting through TrkB receptors), glutamatergic and GABAergic synaptic transmission, transcriptional programmes governing neuronal identity and repair, and gut-brain metabolic signalling that influences nucleus accumbens gene expression.

Research Studies

Intermittent theta burst stimulation and peripheral biomarkers in treatment-resistant depression

Intermittent theta burst stimulation (iTBS) is a non-invasive neuromodulation technique targeting the left dorsolateral prefrontal cortex. A single-centre, prospective, investigator-initiated clinical study is investigating its effects on clinical symptoms, executive functions, and peripheral inflammatory and neuroprotective biomarkers in patients with treatment-resistant depression (TRD) [1]. TRD affects a substantial proportion of patients with major depressive disorder who do not adequately respond to conventional antidepressants, and the biological mechanisms underlying iTBS response remain poorly understood [1]. The study aims to relate changes in peripheral biomarkers to treatment outcomes, positioning neuroplasticity and neuroinflammation as candidate mediators of response [1].

Gut Proteobacteria glycine metabolism and neuroplasticity in cocaine self-administration (mice)

In mice, cocaine exposure altered the composition of the gut microbiome, increasing the abundance of Proteobacteria. This microbial shift led to depletion in host glycine levels, which in turn altered cocaine-induced transcriptional changes in the nucleus accumbens (NAc) and facilitated the development of behavioural sensitization and reinstatement of cocaine self-administration [2]. The findings identify a gut-brain metabolic route by which a bacterial population can regulate neuroplasticity-related gene expression and motivated behaviour in a preclinical model [2].

Cerebrolysin as an adjunct to speech-language therapy in post-stroke Wernicke's aphasia (case report)

A case report described a 38-year-old female lawyer who developed acute Wernicke's aphasia and right-sided hemiparesis following an ischemic stroke. Despite timely thrombolysis and mechanical thrombectomy, she experienced significant neurological deficits. Early multidisciplinary rehabilitation combined with a 10-day course of Cerebrolysin was associated with clinical improvement [3]. The authors propose that Cerebrolysin may enhance recovery through neuroprotection and neuroplasticity, though the single-case design precludes causal inference [3].

Cerebrolysin and language ability in non-fluent aphasia after stroke (randomized trial)

A randomized, placebo-controlled, double-blinded, single-centre study is measuring changes in language ability after adding Cerebrolysin to standard treatment for non-fluent aphasia in patients with post-stroke language impairment. Participants are divided into an experimental group receiving speech therapy plus Cerebrolysin and a control group receiving speech therapy alone; the primary comparison uses PK-WAB scores before and after administration [6]. According to stroke registries cited in the record, 15–42% of patients in the subacute phase and 25–50% of patients with chronic stroke show symptoms of aphasia [6].

Transcriptional rejuvenation of corticospinal neurons and rehabilitation after stroke (mice)

Spontaneous recovery after ischemic stroke is often limited, largely attributed to age-related decline in neuroplasticity. In mice, ectopic expression of a cocktail of transcription factors (Oct4, Sox2, and Klf4, referred to as OSKTFs) reset developmental decline of epigenetic signatures in adult corticospinal neurons without affecting their spinal projection patterns and function in controlling skilled locomotion. Corticospinal expression of OSKTFs had moderate effects on promoting collateral sprouting of corticospinal tract axons and recovery of skilled motor function following a photothrombotic stroke. When combined with task-dependent rehabilitation, the effects were more pronounced [4].

Cytokines and neuroplasticity modulators in spinal canal stenosis and endoscopic decompression

Lumbar spinal stenosis (LSS) is a common degenerative musculoskeletal disorder characterized by narrowing of the spinal canal, often leading to pain and disability. A primary contributor is hypertrophy of the ligamentum flavum (LF), along with facet joint degeneration, intervertebral disc herniation, and ligament ossification; the pathophysiological mechanisms remain incompletely understood. Histological changes in hypertrophied LF include fibrocartilaginous metaplasia, type II collagen proliferation, ossification, calcium crystal deposition, and degeneration of elastic and collagen fibres [5]. A clinical study is examining cytokines and neuroplasticity modulators as biomarkers in this condition and after endoscopic decompression [5].

Psilocybin and psilocybin-assisted cognitive behavioural therapy in major depressive disorder

A randomized controlled clinical trial is evaluating psilocybin and psilocybin-assisted cognitive behavioural therapy (CBT) in the management of major depressive disorder (MDD). The study compares psilocybin-only therapy, CBT, and psilocybin-assisted CBT on depression symptoms, neurochemical markers, inflammatory markers, and neuroplasticity in individuals with MDD. Participants continue their routine depression medications and are assessed for changes in depression scores, biochemical markers, and brain activity patterns using validated tools and tests [7].

Telehealth aerobic exercise and cognitive training after a first schizophrenia episode

In a 12-month randomized controlled trial, all participants receive cognitive training; half are randomly assigned to an aerobic exercise and strength training condition and half to a Healthy Living Group condition. The primary outcome measures are improvement in cognition and level of engagement in in-group and at-home exercise sessions. Increases in serum mature BDNF, which is associated with greater brain neuroplasticity and is an indicator of engagement in aerobic exercise, are among the assessed markers [8]. The study population comprises patients receiving psychiatric treatment at the UCLA Aftercare Research Program [8].

Reference-only findings

Additional evidence supports the broader context of neuroplasticity research. A review reports that the skin-brain axis is a bidirectional neuroimmune network linking cutaneous inflammation with central neuroinflammation, stress signalling, and behavioural disturbances, and evaluates pharmacological strategies targeting this communication [9]. Another review reports that exercise acts as a biologically active stimulus influencing stress-responsive neural systems across molecular, autonomic, neurochemical, neuroimmune, and network levels, with evidence from human intervention studies and neuroimaging [10]. A further review reports that osteopontin (encoded by secreted phosphoprotein 1) is a multifunctional matricellular phosphoglycoprotein that interacts with microglial priming, vascular remodelling, myelin repair, and innate immune responses during aging [11]. Finally, a randomized controlled trial in 120 patients with subacute spinal cord injury reports that adding a fixed-dose combination of inosine monophosphate, agmatine sulphate, and L-carnosine (CGXNW) to standard care for 6 months was assessed for neurological recovery and functional independence [12].

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