Mind–Body Interventions as Modulators of Neural Connectivity and Cognition in Individuals at Risk for Alzheimer’s Disease: A Systematic Review

Abstract

Background

Alzheimer’s disease (AD) is the leading cause of dementia worldwide, contributing to nearly 60%-70% of dementia cases. Current pharmacological treatments provide limited symptomatic relief and minimal efficacy in altering disease progression, highlighting the need for complementary interventions. Mind-body practices such as yoga and meditation are increasingly explored for preserving cognitive abilities and reducing neurodegenerative risk.

Summary

This systematic review evaluated randomized controlled trials investigating yoga, meditation, and related mind-body interventions on cognitive and neural health in individuals with normal cognition, mild cognitive impairment, or subjective memory decline. Following PRISMA guidelines, studies published up to March 2025 were reviewed. Findings showed improvements in memory, attention, executive functions, mood, and quality of life. Neurobiological benefits included preservation of hippocampal volume, improved functional connectivity, increased brain-derived neurotrophic factor levels, and reduced neuroinflammation markers. However, methodological limitations such as small sample sizes and short intervention durations were common.

Key Message

Mind-body interventions show promising cognitive and neurobiological benefits in populations at risk of AD. Yoga and meditation may serve as feasible, cost-effective complementary approaches alongside conventional therapy. Larger long-term clinical trials are needed to establish standardized protocols and sustained therapeutic effectiveness.

Keywords

Alzheimer’s disease yoga pranayama meditation cognition neural connectivity

Introduction

Alzheimer’s disease (AD) is the most common neurodegenerative condition, responsible for approximately 60%–70% of dementia cases globally, and represents a major public health challenge in the 21st century.^{1, 2} Estimates from the Alzheimer’s Disease International (ADI) World Alzheimer Report indicate that over 50 million individuals were living with dementia worldwide in 2019, with prevalence projected to increase to 152 million by 2050.³ The incidence of dementia is rising rapidly, with a new case occurring every 3 s. Alongside this growing prevalence, the global economic burden of dementia is substantial, with annual costs estimated at approximately $1 trillion, a figure expected to double by 2030, exerting increasing pressure on healthcare systems, social care services and families worldwide.³ The burden is not confined to high-income countries; low- and middle-income nations are witnessing a steep rise in prevalence, contributing to about two-thirds of all dementia cases. The condition is characterised by insidious onset and progressive decline in multiple domains of cognition, including memory, language, executive functioning and visuospatial abilities, ultimately impairing functional independence and quality of life. Neuropathologically, AD is defined by the extracellular accumulation of amyloid-beta (Aβ) plaques and the intracellular aggregation of hyperphosphorylated tau protein, forming neurofibrillary tangles, processes that disrupt neuronal communication, trigger synaptic loss and culminate in widespread neuronal degeneration.^4–6 These hallmark features are further compounded by oxidative stress, mitochondrial dysfunction, excitotoxicity and neuroinflammatory cascades, which amplify the extent of neurodegeneration and contribute to disease progression.^{7, 8} The major neuropathophysiological mechanisms contributing to the onset and progression of Alzheimer’s disease are illustrated in Figure 1. Despite a robust body of scientific inquiry, the precise mechanisms through which these neuropathophysiological processes interact remain incompletely understood, underscoring the complexity of AD as a multifactorial disorder.

In this context, recent research has emphasised the need to understand and mitigate AD progression through enhanced cognitive assessment and intervention. Numerous neuropsychological studies have sought to characterise the cognitive deficits associated with AD, ranging from early episodic memory impairments to more advanced degeneration in executive functions, attention and language.^9–11 These studies highlight that cognitive dysfunction often predates clinical diagnosis by years or even decades, suggesting a long prodromal period where early non-pharmacological interventions might prove effective. Furthermore, neuroimaging and electrophysiological studies have documented alterations in brain networks, reduced connectivity and abnormal patterns of activation in AD patients, reinforcing the need for interventions targeting brain plasticity and cognitive resilience.^12–15 However, a significant limitation across this body of research is the lack of standardised approaches and data borne out of limited integration of complementary therapies with conventional clinical practice. While some trials have investigated the effects of cognitive training, physical exercise and mindfulness-based practices on AD patients, results remain inconsistent due to heterogeneity in methodologies, small sample sizes and insufficient follow-up durations. Moreover, the majority of research has been conducted in Western populations, with limited large-scale studies examining the role of alternative therapy, including accurately administered yoga, pranayama and meditation, which are deeply embedded in the Indian context and hold potential for culturally relevant interventions. This gap underscores the rationale for systematically reviewing the available evidence, not only to consolidate findings but also to highlight the scope and limitations of current approaches in managing cognitive decline in AD.

Given this perspective, complementary therapies such as mind–body practices are receiving increasing scientific attention for their neuroprotective and cognition-enhancing potential. Yoga, with its integrative combination of physical postures, breath regulation and meditation, has been shown to reduce psychological stress, enhance autonomic regulation and increase brain-derived neurotrophic factor (BDNF), a key mediator of synaptic plasticity and memory consolidation.^16–19 Collectively, these approaches hold promise as adjunctive strategies that may complement conventional pharmacological treatments, improve quality of life and potentially delay disease progression. Yet, clinical integration remains constrained by challenges such as methodological inconsistencies, lack of standardisation in yoga protocols and the absence of large-scale, high-quality randomised controlled trials (RCTs). Herein lies the importance of systematic reviews by synthesising disparate lines of evidence; such reviews can critically evaluate the efficacy and safety of these complementary interventions, identify gaps in the current literature and guide future clinical applications. As AD prevalence escalates globally, particularly in ageing societies such as India, interdisciplinary approaches that combine modern biomedical advances with traditional holistic practices may offer a pathway towards more effective prevention and management. The present systematic review is, therefore, undertaken with the aim of addressing this critical need, consolidating the existing evidence on yoga interventions in AD, and providing a framework for future research and clinical integration.

This illustration summarises the various pathophysiological aspects of AD. It develops through a combination of pathological processes that progressively damage the brain. One of the primary causes is the abnormal accumulation of Aβ plaques and protein aggregates, including α-synuclein, which misfold and clump together, disrupting cell-to-cell communication and triggering toxic effects inside neurons. Alongside this, the brain undergoes significant oxidative stress, where excessive reactive oxygen species (ROS) overwhelm the brain’s antioxidant defence. This imbalance damages proteins, lipids and DNA, impairing mitochondrial function and leading to neuronal injury. Another major contributor is blood–brain barrier (BBB) leakage and neuroinflammation. The normally protective BBB becomes compromised, allowing harmful substances to penetrate brain tissue. This activates microglia and astrocytes, causing the release of inflammatory cytokines, which creates a chronic inflammatory environment that accelerates neuronal degeneration. Over time, these insults lead to progressive neuronal loss and degeneration, particularly in memory-related regions such as the hippocampus. The degeneration of hippocampal neurons disrupts memory encoding and retrieval, a hallmark symptom of AD. Finally, these structural and functional changes manifest in abnormal brain wave patterns, including disrupted alpha, beta, theta and delta rhythms, reflecting impaired neural connectivity and communication. Together, the synergistic effects of protein aggregation, oxidative damage, vascular dysfunction, inflammation and neuronal loss drive the onset and progression of AD.

Figure 1.

Source: Created with BioRender.com.

Methods

This review was conducted in accordance with the report review under the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, as shown in Figure 2.

Figure 2.

PRISMA Flowchart of the Included Studies.

Search Strategy

The literature search was conducted independently by two researchers, and disagreements were resolved through consultation and discussion with a third researcher. PubMed, Medline, Scopus, Web of Science, Google Scholar and Cochrane Library databases were searched for RCTs on yoga for AD by combining the MeSH terms and keywords (‘yoga, AD, Cognitive Decline’). The literature search covered studies published over the last 15 years, from January 2010 to 31 March 2025, across all selected databases. Only studies published in English were considered, with no restrictions applied regarding geographical region or sample size. The PubMed search strategy is shown in Table 1.

Table 1.

Search Strategy for Studies.

Database	Search Terms
PubMed	(‘Alzheimer’s Disease’[MeSH] OR ‘Dementia’[MeSH] OR ‘Neurodegenerative Disorders’[MeSH] OR ‘Cognitive Functions’[MeSH] OR ‘Cognitive Decline’[MeSH]) AND (‘Yoga’[MeSH] OR ‘Yoga Therapy’[MeSH] OR ‘Breathing Exercises’[MeSH] OR ‘Meditation’[MeSH] OR ‘Pranayama’ OR ‘Yogic Practices’ OR ‘Asana’ OR ‘Dhyana’) AND (‘Brain Health’ OR ‘Brain Function’ OR EEG OR fNIRS OR MRI OR fMRI OR PET OR SPECT) AND (‘Randomized Controlled Trial’ OR ‘Clinical Trial’ OR ‘intervention studies’)
MEDLINE	Same as PubMed
Scopus	(TITLE-ABS-KEY(‘yoga’ OR ‘yoga therapy’ OR ‘breathing practices’ OR ‘pranayama’ OR ‘meditation’ OR ‘mind-body yogic practices’)) AND (TITLE-ABS-KEY(‘neurodegenerative disorders’ OR ‘Alzheimer’s disease’ OR ‘dementia’ OR ‘cognitive functions’ OR ‘cognitive decline’ OR ‘memory’ OR ‘attention’ OR ‘decision-making’ OR ‘awareness’)) AND (TITLE-ABS-KEY(‘brain health’ OR ‘brain function’ OR EEG OR fNIRS OR MRI OR fMRI OR PET OR SPECT)) AND (TITLE-ABS-KEY(‘randomized controlled trial’ OR ‘clinical trial’ OR ‘intervention study’))
Web of Science	TS = (‘yoga’ OR ‘yoga therapy’ OR ‘breathing practices’ OR ‘pranayama’ OR ‘meditation’) AND TS = (‘neurodegenerative disorders’ OR ‘Alzheimer’s disease’ OR ‘dementia’ OR ‘cognitive functions’ OR ‘cognitive decline’ OR ‘memory’ OR ‘attention’ OR ‘decision-making’ OR ‘awareness’) AND TS = (‘brain health’ OR ‘brain function’ OR EEG OR fNIRS OR MRI OR fMRI OR PET OR SPECT) AND TS = (‘randomized controlled trial’ OR ‘clinical trial’ OR ‘intervention study’)
Google Scholar	(‘Yoga’ OR ‘Yoga therapy’ OR ‘Breathing practices’ OR ‘Pranayama’ OR ‘Meditation’) AND (‘Neurodegenerative disorders’ OR ‘Alzheimer’s disease’ OR ‘Dementia’ OR ‘Cognitive functions’ OR ‘Cognitive decline’ OR ‘Memory’ OR ‘Attention’) AND (‘Brain health’ OR ‘Brain function’ OR EEG OR fNIRS OR MRI OR fMRI OR PET OR SPECT) AND (‘Randomized Controlled Trial’ OR ‘Clinical Trial’ OR ‘Intervention study’)
Cochrane Library	(‘Yoga’ OR ‘Yoga therapy’ OR ‘Breathing practices’ OR ‘Pranayama’ OR ‘Meditation’) AND (‘Neurodegenerative disorders’ OR ‘Alzheimer’s disease’ OR ‘Dementia’ OR ‘Cognitive functions’ OR ‘Cognitive decline’) AND (‘Memory’ OR ‘Attention’ OR ‘Brain health’ OR ‘Cognitive outcomes’) AND (‘Randomized Controlled Trial’ OR ‘Clinical Trial’ OR ‘Intervention study’)
Embase	(‘neurodegenerative disorder’/exp OR ‘Alzheimer’s disease’/exp OR ‘dementia’/exp OR ‘cognitive function’/exp OR ‘cognitive decline’/exp) AND (‘yoga’/exp OR ‘yoga therapy’/exp OR ‘breathing exercise’/exp OR ‘pranayama’/exp OR ‘meditation’/exp) AND (‘brain health’/exp OR ‘brain function’/exp OR EEG OR fNIRS OR MRI OR fMRI OR PET OR SPECT) AND (‘intervention studies’/exp OR ‘randomized controlled trial’/exp OR ‘clinical trial’/exp)

Eligibility Criteria

The present systematic review aimed to synthesise high-quality evidence on the effects of yoga, meditation and other mind–body interventions on cognitive function, neural connectivity and AD risk among older adults. Studies were included if they met the following criteria: (a) RCT design; (b) participants at risk of AD, including those with subjective cognitive decline (SCD), mild cognitive impairment (MCI) or other preclinical cognitive risk states; (c) interventions involving yoga, meditation or integrated mind–body practices; and (d) reported pre- and post-intervention assessments of cognitive, behavioural or neuroimaging outcomes. Only peer-reviewed studies published in English were considered to maintain methodological rigour, ensure accessibility for evaluation and avoid potential inaccuracies associated with the translation of non-English publications. Exclusion criteria included studies with animal models, non-yogic physical exercise interventions, pharmacological treatments, or participants with major neurological, psychiatric or systemic illnesses that could confound cognitive outcomes. Grey literature, including conference abstracts, dissertations, reports and non-peer-reviewed materials, was excluded to ensure methodological rigour, transparency and reproducibility of the findings. In addition, conference abstracts and review articles were not included, as abstracts often lack sufficient methodological detail for critical appraisal, and reviews do not provide primary data necessary for quantitative or mechanistic synthesis. The inclusion and exclusion parameters were systematically applied to ensure that only relevant, methodologically sound and outcome-focused studies were analysed. The detailed selection process and specific criteria are summarised in Table 2, providing transparency and replicability.

Table 2.

Criteria to Include or Exclude Studies for the Present Study.

Parameter	Inclusion Criteria	Exclusion Criteria
Population	Individuals across the AD continuum, including SCD, MCI, individuals at risk for AD, caregivers of AD patients and patients diagnosed with AD	Young (<18 years) subjectsAny person with Parkinson’s disease
Intervention	Any form of yoga, breathing and meditation	Tai chi, Naturopathy, Ayurveda, Unani, Marma or any other complementary therapy other than yoga
Comparison	Methods of comparison, such as forced yoga, breathing, meditation, or control groups (active interventions, no intervention)
Outcomes	Together with a psychological/cognitive outcome, there are neurophysiological outcomes relating to the cardio-respiratory system, central nervous system and autonomic nervous system (i.e., EEG, fMRI, HRV, RSA, ECG and cardio-respiratory synchronisation) measured either during the application of yoga, breathing techniques and meditation following a prolonged intervention	Physiological and psychological/cognitive parameters seem monotonous
Study design	Randomised controlled trial design studies	Reports on cases, longitudinal without randomisation, quasi-experimental design, all types of review articles, including critical review, narrative, perspective, systematic, comprehensive reviews, protocol study, inadequate explanation of the experimental setup and procedures hinders the possibility of replication

Note: AD, Alzheimer’s disease; ECG, electrocardiography; EEG, electroencephalography; fMRI, functional MRI; HRV, heart rate variability; MCI, mild cognitive impairment; RSA, respiratory sinus arrhythmia; SCD, subjective cognitive decline.

Study Screening and Data Extraction

Study selection for the present systematic review was independently conducted by two different reviewers to ensure methodological rigour and minimise selection bias. The process followed a two-stage approach in accordance with PRISMA guidelines. In the first stage, titles and abstracts of all retrieved articles were carefully screened to identify studies that met the preliminary inclusion criteria. In the second stage, full-text articles of the shortlisted studies were reviewed in detail to confirm their eligibility for inclusion. Any discrepancies or disagreements between the two reviewers were resolved through discussion and mutual consensus to maintain objectivity and accuracy.

Data extraction was performed systematically using a standardised template designed to capture comprehensive study characteristics. Extracted information included participant demographics (such as age, sex and clinical diagnosis), methodological details (including randomisation procedures and study design), specifics of the intervention (type of yoga, frequency, duration and session structure), and details of the control or comparison group (type, frequency and duration of activity). Outcome measures were recorded based on validated assessment tools evaluating cognitive performance, psychological well-being, neuroimaging findings or other relevant parameters. This structured and transparent screening and data extraction process ensured consistency, reproducibility and high-quality evidence synthesis for the review.

Quality Assessment

The methodological quality and internal validity of the included studies were critically appraised using the Cochrane Risk of Bias 2 (RoB 2) tool, which provides a comprehensive and standardised framework for evaluating potential sources of bias in RCTs. This tool assesses five key domains: bias arising from the randomisation process, bias due to deviations from intended interventions, bias resulting from missing outcome data, bias in the measurement of outcomes, and bias in the selection or reporting of results. Each domain was independently reviewed by two authors to ensure accuracy and consistency in assessment. Any discrepancies were resolved through discussion and consensus.

Based on the Cochrane recommendations, the overall risk of bias for each study was categorised as low risk, some concerns, or high risk depending on the extent and nature of identified methodological limitations. This systematic evaluation ensured a transparent appraisal of study quality, enhancing the credibility and reliability of the synthesised findings. The risk of bias summary is depicted in Figure 3, and the risk of bias graph is shown in Figure 4.

Figure 3.

Risk of Bias Summary: A Review of the Authors’ Judgments About Each Risk of Bias Item for Each Included Study.

Figure 4.

Risk of Bias Graph: Review Authors’ Judgements About Each Risk of Bias Item, Presented as a Percentage of Included Studies.

Results

This synthesis of randomised and comparative intervention studies examines the effects of mind–body practices on cognitive, psychosocial, neuroimaging and biological outcomes in individuals with SCD, MCI, early AD and older adults at risk of cognitive deterioration. Across the included studies, sample sizes ranged from small mechanistic pilot investigations to moderate-sized RCTs, reflecting a methodological spectrum that balances exploratory neurobiological research with clinically oriented intervention studies. Most interventions were delivered over 8–12 weeks, consistent with standardised protocols for mindfulness-based stress reduction (MBSR), Kundalini Yoga (KY), Kirtan Kriya (KK), mindfulness awareness practices and chair yoga. Outcome assessments were multidimensional, integrating subjective memory measures, objective neuropsychological tests, psychosocial scales and advanced biological indices such as structural and functional neuroimaging, inflammatory markers, telomere biology, Aβ levels and gene expression profiles. Collectively, the studies demonstrate that mind–body interventions are feasible, safe and well-tolerated in cognitively vulnerable and older populations, including those with physical or mobility limitations, as evidenced by the successful implementation of chair-based and online yoga programmes.

Across cognitive and psychosocial domains, included studies indicate consistent improvements in subjective memory, perceived stress, mood, sleep quality, resilience and quality of life following mind–body interventions, often equalling or surpassing outcomes observed in active control conditions. While objective cognitive test improvements were generally modest, stabilisation or attenuation of decline was frequently observed, suggesting a role in supporting cognitive resilience rather than producing large short-term cognitive gains. Moreover, studies incorporating neuroimaging and molecular outcomes revealed distinct neurobiological effects associated with mind–body practices that were not consistently evident in cognitive training-based comparators. These included preservation in hippocampal and grey matter volume, enhanced hippocampal–posterior cingulate cortex connectivity, improved DMN integrity and reduced indicators of cortical atrophy. At the molecular level, mind–body practices were associated with increased telomerase activity, maintenance of telomere length, modulation of plasma Aβ concentrations, stabilisation of inflammatory markers such as eotaxin-1, and favourable shifts in ageing- and immune-related gene expression pathways. Markedly, several studies reported correlations between biological improvements and gains in memory, stress reduction or psychosocial well-being, lending mechanistic plausibility to observed clinical effects. When contrasted with memory enhancement training, yoga and meditation appeared to preferentially influence stress-sensitive neural circuits, inflammatory regulation and ageing-related biological processes, whereas cognitive training primarily affected task-specific cognitive performance. Overall, synthesised studies support the interpretation that mind–body practices exert multisystem benefits spanning psychological, neural and molecular levels, positioning them as promising complementary, non-pharmacological strategies for promoting cognitive resilience and potentially slowing neurodegenerative processes in at-risk ageing populations.

Discussion

AD and its prodromal conditions, including MCI and SCD, represent a continuum of neurodegenerative conditions. The studies mentioned in Table 3 collectively explore a wide array of variables that contribute to our understanding of AD pathophysiology, diagnosis and intervention. This discussion synthesises these variables into a coherent narrative, emphasising their interrelationships and clinical relevance.

Table 3.

Characteristics of the Included Studies.

Author(s) and Year	Study Population	Sample Size	Variables	Intervention Experimental	Comparison	Duration of Intervention	Outcomes
Innes et al. (2018)²⁰	Older adults with SCD	60	MFQ, DSST, TMT, PSS, POMS, PWB, PSQI, QOL, TL, TA, Plasma Aβ	Kirtan Kriya Meditation Program	Music listening programme	12 weeks	Both interventions improved cognitive function, mood, sleep and quality of life in adults with subjective cognitive decline. Both increased telomerase activity and telomere length, while Kirtan Kriya showed greater rises in plasma Aβ40. Biomarker improvements correlated with better memory and psychosocial outcomes
Grzendra et al. (2024)²¹	Older women at risk for AD	79	MFQ, HVLT-R, WMS-IV, SIT, TMT, BDI, HAM-A, CD-RISC-25, PSS, CCL, RNAS	Kundalini Yoga	Memory enhancement training	12 weeks	Kundalini Yoga improved subjective memory, particularly reducing the seriousness of forgetting. Yoga participants showed anti-ageing gene expression changes and stable eotaxin-1 levels, while memory training increased this ageing marker. Both groups improved in perceived memory, mood and resilience, but yoga uniquely modulated inflammatory pathways
Sánchez-Pérez et al. (2024)²²	Patients with AD and their caregivers	66	HADS, NPI-Q, GDS	MBHC	Treatment as usual (TAU)	8 weeks	No significant improvements occurred in patients’ behavioural or psychological symptoms. Mindfulness training proved feasible and beneficial in the short term
Wells et al. (2013)²³	Individuals with MCI	14	DMN, HV, ADAS-Cog	MBSR	Non-meditator	8 weeks	MBSR enhances brain function in mild cognitive impairment. MBSR improved DMN connectivity and showed less hippocampal atrophy versus controls, suggesting meditation may positively influence brain regions vulnerable to AD progression
Krause-Sorio et al. (2022)²⁴	Older women at risk for AD	26	GMV, CDR, MMSE, MFQ, BDI, HAM-A, BDI, HAM-A, CD-RISC, PSS, SERS	KY + KK	MET	12 weeks	Yoga participants showed preserved grey matter and increased right hippocampal volume, while the memory training group exhibited cortical atrophy. Yoga also improved anxiety and depression, indicating potential neuroprotective benefits
Kaushik et al. (2025)²⁵	Patients with AD and caregivers	30	MMSE, ADAS-Cog, PSS, QoL-AD, RS, HHI, LOT-R, fMRI	MBSR	Stress education	12 weeks	MBSR improves functional connectivity between the hippocampus and posterior cingulate cortex compared to stress education. Findings suggest mindfulness may strengthen neural connectivity related to memory and stress regulation
Innes et al. (2012)²⁶	Patients with AD and caregivers	12	MMSE, ADAS-Cog, fMRI	MAP	HEP	8 weeks	Participants in the mindfulness group showed improved hippocampal functional connectivity and stable cognitive performance compared to the health education control group, suggesting meditation may support brain function and delay cognitive decline
Park et al. (2019)²⁷	Community-dwelling older adults with dementia	27	mini-PPT, SPPB, TUG, BMI, PSQI, ESS, QoL	CY, CYE	MI	12 weeks	Chair yoga and exercise improved physical performance and quality of life more than music intervention, demonstrating safe, feasible nonpharmacological dementia therapies
Park et al. (2025)²⁸	Older adults at risk for AD	32	Mini-MoCA, TUG, PSPIM, LS, CCQ	OCY	CBG	8 weeks	Both groups improved cognitive and physical performance, but yoga participants showed greater reductions in pain and mobility time. Findings suggest online chair yoga is a feasible, effective intervention for enhancing well-being in older adults
Kilpatrick et al. (2023)²⁹	Older women at risk for AD	63	PSS, MFQ, BDI, HAM-A, rs-fMRI	KY + KK	MET	12 weeks	Yoga improved stress-related anterior hippocampal connectivity, while MET enhanced sensory-based hippocampal connectivity linked to memory reliability. Findings suggest yoga benefits stress-sensitive brain pathways supporting cognitive resilience

Note: ADAS-Cog, cognitive performance; BDI, Beck Depression Inventory; BMI, body mass index; CBG, chair-based group exercise; CCL, cytokine and chemokine levels; CDR, Clinical Dementia Rating Scale; CD-RISC-25, Connor-Davidson Resilience Scale; CY, chair yoga; DMN, default mode network; DSST, Digit Symbol Substitution Test; ESS, Epworth Sleepiness Scale; fMRI, functional MRI; GDS, Global Deterioration Scale; GMV, grey matter volume; HADS, Hospital Anxiety and Depression Scale; HAM-A, Hamilton Anxiety Rating Scale; HEP, health education programme; HHI, Herth Hope Index; HV, hippocampal volume; HVLT-R, Plasma Aβ, Hopkins Verbal Learning Test-Revised; KY + KK, Kundalini Yoga combined with Kirtan Kriya; LOT-R, Life Orientation Test–Revised; LS, Loneliness Scale; MAP, mindfulness awareness practice; MBSR, mindfulness-based stress reduction; MBHC, Mindfulness-Based Health Care Program; MCI, mild cognitive impairment; MET, memory enhancement training; MFQ, Memory Functioning Questionnaire; MI, music intervention; Mini-MoCA, Mini-Montreal Cognitive Assessment; mini-PPT, Mini Physical Performance Test; MMSE, Mini-Mental State Examination; NPI-Q, Neuropsychiatric Inventory Questionnaire; OCY, online chair yoga; POMS, Profile of Mood States; PSS, Perceived Stress Scale; PSPIM, Pain Scale and Pain Interference Measures; PSQI, Pittsburgh Sleep Quality Index; PWB, Psychological Well-Being Scale; QoL, quality of life; QoL-AD, quality of life–Alzheimer’s disease; RNAS, RNA sequencing; RS, Resilience Scale; rs-fMRI, resting-state MRI; SERS, UKU Side Effect Rating Scale; SIT, Stroop Interference Test; SPPB, short physical performance battery; TA, telomerase activity; TL, telomere length; TMT, Trail-making Test; TUG, Timed Up and Go Test; WMS-IV, Wechsler Memory Scale-IV.

The Neural Landscape of Cognition in Alzheimer’s Disease

The progressive neurodegenerative disorder AD is characterised by the accumulation of Aβ plaques and hyperphosphorylated tau neurofibrillary tangles, leading to widespread synaptic and neuronal dysfunction. In the early stages of AD, neurodegeneration predominantly affects the hippocampus and entorhinal cortex, regions critical for episodic memory formation and spatial navigation, resulting in impairments in memory consolidation and retrieval.^{30, 31} As the disease progresses, tau pathology propagates along anatomically connected networks, producing progressive cortical atrophy detectable via structural neuroimaging and manifesting as escalating cognitive decline.³²

Beyond gross neurodegeneration, synaptic dysfunction represents an early and central pathological feature of AD. Tau pathology disrupts microtubule stability and postsynaptic density organisation, leading to dendritic spine loss, impaired synaptic plasticity and altered neurotransmission. These changes precede overt neuronal loss and are strongly associated with early cognitive impairment.^{33, 34} Electrophysiological studies further demonstrate that AD is associated with disrupted neural oscillatory activity, including reduced gamma and theta synchronisation, impaired cross-frequency coupling and diminished network coherence, all of which are essential for coordinated cognitive processing and memory integration.^{34, 35}

Importantly, several modifiable neural and physiological risk factors implicated in AD pathophysiology overlap with parameters influenced by yogic practices. These include chronic stress and hypothalamic–pituitary–adrenal (HPA) axis dysregulation, autonomic imbalance characterised by reduced vagal tone, neurovascular dysfunction, impaired cerebral blood flow (CBF), chronic low-grade neuroinflammation and altered electrophysiological rhythms.^{36, 37} Dysregulation of these systems exacerbates synaptic vulnerability, accelerates tau propagation and compromises neurovascular coupling, thereby amplifying cognitive decline.

Emerging evidence suggests that yoga-based interventions encompassing asanas, pranayama and dhyana may beneficially modulate several of these AD-relevant mechanisms, including autonomic regulation, cerebral perfusion, stress reactivity, inflammatory signalling and functional neural connectivity.^{38, 39} Thus, targeting these interconnected neural correlates through yoga may offer a plausible complementary strategy to mitigate cognitive deterioration and support neural resilience in AD.

Recent yoga intervention studies have aligned with this neural landscape in individuals at risk for AD and showed promising results for both brain structure and subjective cognitive complaints. RCTs in older women at risk for AD have demonstrated that KY, compared to active memory training, led to long-term improvements in perceived memory function, particularly for the ‘seriousness of forgetting’ domain, as well as stabilisation of executive function.²¹ Neuroimaging data revealed that yoga participants had less grey matter atrophy across widespread cortical regions over 12 weeks, with some evidence for increased hippocampal volume, a region crucial for memory.²⁴ Other studies report that mind–body interventions lower levels of blood stress markers and pro-inflammatory cytokines, and may increase beneficial BDNFs and support telomere maintenance, factors crucial for neuronal health and cognitive resilience.²⁰ These improvements typically co-occur with enhancements in mood, perceived stress and quality of life, supporting a multifaceted impact of yoga on risk pathways relevant to AD and cognitive ageing. Although longer trials and more diverse populations are needed, the available data suggest that yoga is a feasible, safe and biologically plausible non-pharmacological intervention for cognitive protection and brain health in older adults at heightened risk for dementia.^{21, 24}

Hippocampal Structure and Memory Performance

The hippocampus plays a central role in memory formation, consolidation and retrieval, along with spatial navigation, a function critically compromised in AD. Pathological hallmarks of AD, including Aβ plaque deposition and tau neurofibrillary tangles, preferentially affect the hippocampal formation and adjacent entorhinal cortex at early disease stages, leading to pronounced neuronal loss, synapse degeneration and progressive atrophy.⁴ This anatomical decline correlates strongly with worsening clinical memory deficits observed in AD patients.⁴⁰ Structural MRI studies consistently show hippocampal volume reduction in AD and in individuals with MCI, a prodromal stage of AD. Smaller hippocampal volumes especially predict poorer performance on total recall tasks, while hypofunction in the entorhinal cortex relates to impairments in delayed recall.⁴¹ Diffusion-based neuroimaging further reveals disrupted structural connectivity between the hippocampus and multiple large-scale networks, particularly the default mode network (DMN), compromising the integrative processing required for episodic memory. Functional imaging shows metabolic hypofunction even preceding overt hippocampal volume loss, indicating that synaptic or cellular dysfunction manifests initially as decreased CBF or glucose metabolism in these regions.⁴²

Yoga and meditation are beneficial for hippocampal structure and function through several mechanisms. Numerous neuroimaging findings reported that yoga interventions facilitate hippocampal connectivity and volume, which are critical for memory and are notably vulnerable in AD.^{20, 23} A previous study showed that regular yoga practices have been shown to lead to improvements in cognitive function, particularly in domains like attention, language, orientation and delayed recall.^{25, 29} Research shows that yoga and meditation help maintain focused attention and mental awareness, stimulating the hippocampus and supporting brain plasticity while protecting against age- and disease-related decline. Numerous studies of meditation practitioners reveal greater hippocampal activity and grey matter density compared to controls, consistent with enhanced structural and functional preservation.^{43, 44} Yoga-based studies reported that yoga enhances the expression of BDNF and related growth factors that promote neurogenesis, synaptic plasticity and dendritic complexity within the dentate gyrus and CA1-CA3 subfields of the hippocampus.¹⁶ Increased BDNF availability supports the stabilisation and formation of new synaptic connections, directly improving memory encoding and retrieval capabilities. A previous study reported that yoga practices modulate neuroendocrine stress responses, notably by reducing chronic elevation of cortisol, a neurotoxic glucocorticoid that accelerates hippocampal cell loss and dendritic atrophy.⁴⁵ Long-term stress reduction through yoga diminishes the excitotoxic and pro-apoptotic effects of cortisol on hippocampal neurons, thus preserving volume and cellular integrity. The reduction of neuroinflammation via yoga’s immunomodulatory effects protects hippocampal neurons from inflammatory insults that exacerbate AD pathology. This may need long-term yoga and meditation studies that probe the conversion rate of MCI into AD. Lower levels of pro-inflammatory cytokines and oxidative stress maintain synaptic integrity and neuronal health in hippocampal circuits crucial to memory.⁴⁶ Together, these postulated mechanisms illustrate how yoga and meditation create a neuroprotective environment for the hippocampus, attenuating volume loss, sustaining metabolic function and strengthening plasticity, which might translate into slowed memory decline and better episodic memory performance in AD and at-risk individuals.

Default Mode Network Dysfunction and Cognitive Symptoms

The DMN is a central, large-scale brain network that plays a pivotal role in higher cognitive functions such as autobiographical memory, self-referential thinking, episodic memory and mental simulation.⁴⁷ Key centres of the DMN include the medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), precuneus, inferior parietal lobules and bilateral hippocampi. In healthy brains, the DMN exhibits a characteristic pattern of high activity during rest and decreases its activity during goal-directed tasks, demonstrating an antagonistic relationship with task-positive networks (such as the frontoparietal control network), which activate during attention-demanding processes.⁴⁸ In AD, early and progressive disruption of the DMN is well-documented. Aβ deposition preferentially accumulates within DMN nodes, particularly the PCC and the hippocampus, leading to reduced metabolism, synaptic dysfunction and loss of connectivity between these specialised regions.^{49, 50} A previous study reveals diminished coherence within the DMN, alongside a failure to appropriately suppress DMN activity during cognitive tasks, contributing to impairments in memory retrieval, self-monitoring and executive control functions.⁵¹ The progressive loss of normally anti-correlated interactions between the DMN and other large-scale brain networks leads to aberrant hyperactivity within DMN nodes, which paradoxically compromises network flexibility and reduces the efficiency of information processing. Mechanistically, the deterioration of DMN connectivity in AD is linked to synaptic loss, white matter tract degradation (notably those interconnecting hippocampus and cortical DMN regions), and disrupted neurotransmission due to amyloid and tau pathology. This dysconnectivity correlates strongly with cognitive decline severity and predicts progression from MCI to clinical AD.

Emerging evidence suggests that yoga-based practices may modulate DMN activity and connectivity. These practices engender enhanced synchrony of neural oscillations, particularly within the alpha frequency band, fostering greater temporal coordination among DMN centres.⁵² By cultivating sustained attention and mindfulness, meditation downregulates maladaptive DMN hyperactivity and restores dynamic switching capability between rest and task-related network states.^{53, 54} Suppression of excessive spontaneous cognitive activity supports improved attentional stability and metacognitive monitoring. Mind–body practices have been shown to increase DMN functional connectivity, especially between the PCC and hippocampus, reinforcing memory-related circuit integrities.⁵⁵ Improved coupling of anterior and posterior DMN nodes supports integration of self-referential information and contextual memory. Functional neuroimaging demonstrates that these connectivity enhancements manifest as better performance on attention and executive functioning tasks, reduced cognitive intrusions and sustained episodic memory retrieval. Thus, yoga and meditation act as ‘neural integrators’, promoting balanced DMN dynamics, resilient network organisation and enhanced top-down regulation of cognition. By counteracting the progressive DMN fragmentation characteristic of AD, these mind–body practices offer a promising avenue for preserving cognitive faculties and delaying disease manifestations.

Sensory-motor Networks and Multimodal Integration

The sensory-motor system is critical for integrating multisensory input with motor output, supporting not only movement and balance but also the complex cognitive processes involved in perceiving, processing, and responding to environmental stimuli.⁵⁶ In AD, widespread pathology extends beyond memory circuits and disrupts these sensory-motor and multisensory integration networks, contributing to impairment in gait, balance and higher-order cognitive functions such as attention and visuospatial skills.^{57, 58} Audiovisual and multisensory integration requires efficient functional connectivity among brain regions, including the superior temporal sulcus (STS), primary sensory cortices, superior colliculus and cerebellum. These centres form loops for processing temporal and spatial aspects of sensory information and orchestrate appropriate motor responses. In AD, disrupted connectivity and metabolic dysfunction within these regions degrade the brain’s ability to integrate sensory inputs effectively, contributing to slowed motor responses, poor balance, increased fall risk and reduced cognitive processing speed.^{57, 58}

Mind–body practices positively influence the sensory-motor and multimodal integration system through several neurobiological pathways. The components of yoga, such as the physical postures (asanas) and breath regulation (pranayama), stimulate functional activation of primary somatosensory and motor cortices, as well as secondary association areas responsible for proprioception and sensory feedback.⁵⁹ This activation strengthens underlying structural connectivity, reinforcing white matter tracts such as the corticospinal tract and corpus callosum, thus supporting motor coordination. Another component of yoga is meditative practices that enhance interoceptive awareness by engaging the insular cortex, a multimodal centre integrating internal bodily states with cognitive and affective processes.^60–62 This heightened body awareness optimises autonomic regulation and facilitates the dynamic balance of excitatory and inhibitory signalling needed for smooth sensorimotor execution and adaptive responses to complex environments. Mind–body practices improve top-down attentional control via enhanced prefrontal cortex activity, which modulates sensory gating and selective attention mechanisms that prioritise relevant multisensory stimuli.⁶³ This cognitive enhancement allows for more effective monitoring and integration of sensory inputs into coordinated, goal-directed motor activity.⁶⁴ Collectively, these interventions promote a bidirectional synergy where ‘bottom-up’ sensory stimulation via movement and breath work complements ‘top-down’ attentional modulation, resulting in stronger multisensory integration. Clinically, this translates into improvements in balance, gait, fall prevention and cognitive functions related to sensory processing and executive control.^{65, 66} By targeting these sensory-motor and multimodal networks, yoga and meditation address a dimension of AD pathology that is often neglected, linking motor function preservation with cognitive health and independence. Hence, mind–body practices strengthen the sensory-motor network and enhance multimodal sensory integration through activation of cortical and subcortical centres, improved structural and functional connectivity, interoceptive awareness and cognitive control, thereby mitigating motor and cognitive deficits associated with AD.

Increased Cerebral Blood Flow and Oxygenation

One of the consistent observations in AD is reduced CBF, especially in brain regions essential for memory and cognition, including the hippocampus, medial temporal lobe and parietal cortex. Reduced perfusion exacerbates neuronal energy deficits, impairs metabolic function and promotes the accumulation of toxic metabolites like Aβ, accelerating neurodegeneration and cognitive decline.^{67, 68} Mechanistically, AD-associated vascular dysfunction arises due to amyloid deposition in cerebral vessels (amyloid angiopathy), endothelial dysfunction and diminished neurovascular coupling, thereby restricting oxygen and nutrient delivery to vulnerable brain regions.^69–72

Mind–body practices improve CBF and oxygenation through a complex interplay of physiological mechanisms. Breath regulation techniques in yoga (pranayama), including slow deep breathing and alternate nostril breathing, enhance autonomic parasympathetic tone while reducing sympathetic overactivity.⁷³ This autonomic balance leads to vasodilation and improved cerebral vessel responsiveness, which increases regional cerebral perfusion. Functional neuroimaging studies show increased CBF in the prefrontal cortex, hippocampus and other memory-related structures following mind–body practices.⁷⁴ Another study reported that physical postures and gentle movements in yoga augment cardiovascular health by lowering blood pressure, reducing arterial stiffness and improving endothelial function.⁷⁵ These improvements in vascular health promote sustained delivery of oxygenated blood and glucose to metabolically active neurons. Enhanced oxygenation directly fuels mitochondrial respiration in neurons, supporting ATP production critical for synaptic transmission, plasticity and neural repair processes.⁷⁶ Increased CBF also facilitates glymphatic clearance, the brain’s waste removal system active primarily during sleep, which clears neurotoxic substances such as Aβ peptides. Mind–body practices have been associated with improved sleep quality and better glymphatic function, compounding the benefits on amyloid clearance.^{77, 78} Moreover, improved CBF supports the upregulation of neurotrophic factors and the maintenance of BBB integrity, protecting neurons from neurotoxic agents and inflammatory assaults prevalent in AD.

Integrative Mechanistic Pathways Linking Yoga to Neurocognitive Preservation in Alzheimer’s Disease

An integrative mechanistic account elucidates the pathways through which yoga-based mind–body practices may contribute to attenuation of cognitive decline in AD by engaging interacting neuroendocrine, neurotrophic, autonomic-vascular and large-scale brain network processes. A central pathway begins with stress regulation, chronic psychosocial stress drives sustained activation of the HPA axis, producing elevated cortisol that preferentially impairs hippocampal neurons and accelerates atrophy, changes strongly implicated in memory loss and AD progression.⁷⁹ Reducing HPA hyperactivity, therefore, protects hippocampal structure and function, forming a direct link between stress modulation and cognitive preservation.⁸⁰

Convergent evidence supports a neurotrophic route in which contemplative and movement-based practices increase circulating BDNF, a key mediator of synaptic plasticity and hippocampal resilience. Increases in BDNF enhance dendritic complexity, long-term potentiation and the capacity for experience-dependent remodelling, mechanisms that underlie improvements in episodic memory and executive processes.^{81, 82} Mind–body interventions thus provide a biologically plausible means to augment neuroplasticity in vulnerable medial temporal circuits. Meta-analytic and interventional studies report BDNF elevations following sustained yoga/meditation and other mind–body interventions, supporting this mechanistic link.

A complementary vascular-autonomic pathway connects breathing practices and slow, regulated movement to neurovascular coupling and cerebral perfusion. Pranayama and slow-breathing techniques modulate autonomic balance, which in turn favourably influences cerebrovascular dynamics and endothelial function.^{83, 84} It may be due to changes in neurovascular coupling, which is essential for maintaining metabolic support to active networks. Improved autonomic regulation preserves haemodynamic responsiveness and mitigates the neurovascular uncoupling seen early in AD. These autonomic effects may facilitate preservation of regional CBF, especially in hippocampal and posterior cortical nodes, supporting neuronal metabolic demands, clearance of metabolic by-products and functional integrity. At the systems level, mind–body practices modulate the DMN, a large-scale circuit centrally implicated in episodic memory and self-referential cognition and selectively vulnerable in AD. Empirical studies using resting-state fMRI indicate that mindfulness and meditation can enhance DMN connectivity or restore appropriate DMN-task-positive network dynamics, thereby improving network segregation and the capacity to shift between internally and externally focused states.⁵² Enhanced hippocampal-posterior cingulate coupling associated with these practices may contribute to improved memory retrieval and reduced intrusive mind-wandering, thereby supporting cognitive efficiency in AD. These mechanisms operate in an interrelated manner, wherein attenuation of cortisol exposure and upregulation of BDNF promote hippocampal plasticity, improved autonomic regulation sustains the neurovascular support necessary for such plasticity and stabilised network dynamics enhance compensatory recruitment, collectively strengthening cognitive reserve. This integrative model synthesises the heterogeneous empirical effects of yoga into a unified, testable mechanistic framework and underscores the need for multimodal trials combining endocrine measures, neurotrophic markers such as BDNF, autonomic and CBF indices, and network-level neuroimaging to map causal relationships between yoga practice and cognitive preservation in AD.

Future research in this area should focus on conducting large-scale, multicentre RCTs with standardised yoga protocols and longer follow-up periods to validate preliminary findings and assess sustainability. Investigating the neurobiological mechanisms underlying yoga’s benefits through neuroimaging and biomarker analyses can elucidate how these interventions influence brain plasticity, neuroinflammation and cognitive reserve. Additionally, expanding research to encompass diverse cultural populations, including settings where traditional practices like Ayurveda and yoga are deeply rooted, will enhance the generalisability of outcomes. Exploring the synergistic effects of yoga combined with other lifestyle modifications or pharmacological treatments holds promise for a comprehensive management approach. Moreover, examining the impact of yoga on caregiver burden and overall family dynamics can support a holistic approach to dementia care. In light of current limitations, such as heterogeneity in interventions, small sample sizes and potential bias, strict methodological rigour, standardisation and transparent reporting are imperative to advance the evidence base and facilitate clinical translation. Briefly, integrating yoga and meditation into multidimensional management strategies offers a promising, culturally adaptable pathway towards improving quality of life and potentially delaying the progression of AD.

The limitations of existing studies primarily include small sample sizes, short durations of intervention, and heterogeneity in protocols, outcome measures and participant characteristics, which restrict the ability to generalise findings and draw definitive conclusions. Many studies also lack long-term follow-up data necessary to determine sustained benefits. The risk of bias due to inadequate blinding, lack of proper control groups and reliance on subjective assessments further complicates interpretation. Additionally, most research has been conducted in Western populations, limiting cultural applicability and relevance in regions where traditional practices like yoga are integral to health. The lack of standardised and validated intervention protocols and inconsistent reporting standards also hinders comparability across studies.

Conclusion

Mind–body interventions offer numerous cognitive benefits for individuals with AD by supporting brain health and slowing cognitive decline. Research shows that yoga may improve attention, memory, executive function and overall cognitive performance through multiple neurobiological mechanisms. Regular yoga practice may enhance hippocampal volume and connectivity, a critical brain region compromised early in AD, which underlies memory consolidation and retrieval. Yoga may increase BDNF, supporting neurogenesis and synaptic plasticity essential for maintaining cognitive function. Importantly, yoga may reduce chronic stress and lower cortisol levels, mitigating neurotoxic effects on hippocampal neurons. Functional neuroimaging studies reveal improved activity and synchronisation within the DMN, which is disrupted in AD and vital for autobiographical memory and self-referential processing. Additionally, yoga might enhance sensory-motor integration and CBF, further supporting cognitive resilience. These combined effects may promote neural plasticity, reduce neuroinflammation and protect against hippocampal atrophy. While more large-scale, long-term trials are needed, current evidence supports yoga as a feasible, safe and effective complementary intervention to enhance cognition and quality of life in AD patients and those at risk, bridging mind–body practices with AD management.

Footnotes

Acknowledgements

The authors sincerely acknowledge Swami Vivekananda Yoga Anusandhana Samsthana (S-VYASA) for providing the academic platform and research environment to conceptualise and prepare this work. They are grateful for the institutional support, scholarly resources and encouragement that facilitated the development of this manuscript.

Authors’ Contributions

Dwivedi Krishna conceived the study, designed the review framework and led the manuscript writing. Avinash Chandra Pandey contributed to the synthesis of results, conceptual guidance and manuscript editing. Saurav Nilesh contributed to the literature search, data extraction and critical appraisal of included studies. Sridam Ananda assisted in methodology formulation and interpretation of neurobiological findings. Jyoti Amit Singh supported data organisation, synthesis of results and manuscript editing. Amit Singh provided overall supervision, conceptual guidance and critical revision of the manuscript for important intellectual content. All authors reviewed and approved the final manuscript.

Declaration of Conflict of Interests

The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Funding

The authors received no financial support for the research, authorship and/or publication of this article.

ICMJE Statement

The manuscript complies with ICMJE guidelines.

Patient Consent

Informed consent was not applicable, as this study is a review based on previously published research and guidelines and did not involve direct participation of human subjects.

Statement of Ethics

Ethical permission was not required for the systematic review research article.

ORCID iDs

Dwivedi Krishna

Jyoti Amit Singh

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