# Tai Chi exercise and neuroplasticity: a narrative review according to neural mechanisms and clinical utilizations in brain health

**Authors:** Xiaoqiang Jin, Juanjuan Chen, Xiaoqi Zhang

PMC · DOI: 10.3389/fnins.2026.1769779 · Frontiers in Neuroscience · 2026-02-19

## TL;DR

This review explores how Tai Chi promotes brain health by enhancing neuroplasticity through physical and mental practices, offering benefits for cognitive, motor, and emotional functions.

## Contribution

The paper provides a comprehensive narrative review linking Tai Chi's effects on neuroplasticity to clinical applications in brain health.

## Key findings

- Tai Chi increases gray matter volume in the hippocampus and prefrontal cortex.
- It enhances brain network organization and promotes synaptic plasticity via BDNF upregulation and improved metabolism.
- Tai Chi shows clinical benefits in neurological rehabilitation, including for Parkinson’s disease and stroke.

## Abstract

Neuroplasticity is the core process by which the brain responds to aging, learning, and injury. Reporting positive non-pharmacological intervention approaches to promote neural plasticity is a core focus of contemporary neuroscience and rehabilitation medicine. Tai Chi (TC), as a traditional Chinese physical and mental practice that deeply combines soothing body movements, breathing regulation, and spiritual focus, is increasingly attracting attention from the scientific community for its role in facilitating brain health.

Our review seeks to combine recent evidence, elucidate how TC promotes neural plasticity via multi-level mechanisms, discuss its advantages in promoting cognitive, motor, and emotional functions, and investigate its clinical utilization prospects and future research challenges in neurorehabilitation.

According to reviewing recent literature, we combined evidence from cross-sectional studies, randomized controlled trials, systematic reviews, and meta-analyses, with a center on citing research findings utilizing multimodal neuroimaging techniques (such as fMRI, fNIRS, EEG) and molecular biology techniques to construct a complete chain of evidence from molecules to systems.

TC drives multi-level neural plasticity modifications via its unique physical and mental combination properties. At the macro level, it can enhance the gray matter volume of the hippocampus and prefrontal cortex, and promote the organizational effectiveness of large-scale functional networks in the brain. At the micro molecular level, TC establishes a favorable microenvironment for neuronal survival, synaptic plasticity, and neural repair by upregulating BDNF, increasing endogenous antioxidant defense, modulating inflammatory balance, and improving mitochondrial energy metabolism. These structural, functional, and molecular level changes collectively form the neurobiological basis for TC to promote memory and executive function, increase balance and motor management, and promote emotional regulation ability. Our review further assesses the clinical effectiveness of TC in the rehabilitation of neurological diseases, such as Parkinson’s disease (PD), stroke, and mild cognitive impairment, determining that it not only decreases symptoms, but may also have the possible role to decrease disease development. Ultimately, our review delve into the challenges and future perspectives experienced by this range in the context of standardization of research paradigms, causal reasoning of mechanisms, and individualized interventions.

## Linked entities

- **Proteins:** BDNF (brain derived neurotrophic factor)
- **Diseases:** Parkinson’s disease (MONDO:0005180), stroke (MONDO:0005098)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, CAT (catalase) [NCBI Gene 847], NTF3 (neurotrophin 3) [NCBI Gene 4908] {aka HDNF, NGF-2, NGF2, NT-3, NT3}, SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL12B (interleukin 12B) [NCBI Gene 3593] {aka CLMF, CLMF2, IL-12B, IMD28, IMD29, NKSF}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}
- **Diseases:** COVID-19 (MESH:D000086382), ischemic stroke (MESH:D002544), fibromyalgia (MESH:D005356), cardiovascular disease (MESH:D002318), neurocognitive disorders (MESH:D019965), osteoporosis (MESH:D010024), muscular imbalances (MESH:D000137), knee osteoarthritis (MESH:D020370), decline in cerebrovascular function (MESH:D002561), rheumatoid arthritis (MESH:D001172), brain injuries (MESH:D001930), impairments in motor function, balance, (MESH:D000068079), Cognitive Impairment (MESH:D003072), TC (MESH:D054463), depression (MESH:D003866), Chronic pain (MESH:D059350), neuronal damage (MESH:D009410), dementia (MESH:D003704), muscular strength (MESH:D009135), enhancement (MESH:C564835), brain atrophy (MESH:C566985), MCI (MESH:D060825), AD (MESH:D000544), atrophy (MESH:D001284), anxiety (MESH:D001007), neuroinflammation (MESH:D000090862), TBI (MESH:D000070642), metabolic syndrome (MESH:D024821), neurodegeneration (MESH:D019636), Chronic inflammation (MESH:D007249), PD (MESH:D010300), pain (MESH:D010146), neurological deficits (MESH:D009461), osteoarthritis (MESH:D010003), difficulty (MESH:D051346), low back pain (MESH:D017116), falls (MESH:C537863), neurological diseases (MESH:D020271), Stroke (MESH:D020521), function (MESH:D003291)
- **Chemicals:** Cr (MESH:D002857), N-acetylaspartate (MESH:C000179), creatine (MESH:D003401), PGE1 (MESH:D000527), PCr (MESH:D010725), MDA (MESH:D008315), levodopa (MESH:D007980), Baduanjin (-), ROS (MESH:D017382), calcium (MESH:D002118), oxylipins (MESH:D054883), ATP (MESH:D000255), endocannabinoids (MESH:D063388), lipid (MESH:D008055), lipid peroxides (MESH:D008054), oxygen (MESH:D010100), AGEs (MESH:D017127), PGE2 (MESH:D015232)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** Val66Met

## Full text

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## Figures

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## References

97 references — full list in the complete paper: https://tomesphere.com/paper/PMC12960153/full.md

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Source: https://tomesphere.com/paper/PMC12960153