Long-term brain health refers to the sustained preservation of cognitive function — including memory, reasoning, attention, and processing speed — across the lifespan. It encompasses the biological, nutritional, and lifestyle factors that determine whether your brain remains resilient as you age or becomes vulnerable to decline.
The evidence is clear: cognitive decline is not an inevitable consequence of ageing. The 2024 Lancet Commission on dementia identified 14 modifiable risk factors that collectively account for approximately 45% of all dementia cases worldwide.1 That means nearly half of dementia risk is within your influence — through the choices you make about diet, exercise, sleep, stress management, social connection, and nutritional support.
Key Takeaways
- The 2024 Lancet Commission found that 14 modifiable risk factors account for roughly 45% of global dementia cases, meaning nearly half of cognitive decline risk is within your control.1
- Physical exercise increases brain-derived neurotrophic factor (BDNF), supporting neurogenesis and synaptic plasticity — the brain's ability to form new connections.2
- The glymphatic system clears neurotoxic waste including amyloid-beta during deep sleep; disrupted sleep accelerates neurodegenerative pathology.3
- Mediterranean and MIND dietary patterns are associated with reduced risk of cognitive impairment and dementia in meta-analyses of cohort studies.4
- Loneliness increases dementia risk by approximately 31% (HR 1.31), independent of depression and social isolation, according to a 2024 meta-analysis of over 600,000 individuals.5
- Omega-3 supplementation shows dose-dependent cognitive benefits, with a 2025 meta-analysis of 58 studies finding significant improvements in attention, perceptual speed, and language at 2,000 mg/day.6
What Does "Long-Term Brain Health" Actually Mean?
Long-term brain health is the capacity of the brain to maintain its core functions — learning, memory, emotional regulation, and executive control — throughout the lifespan. It is shaped by the interplay of neuroplasticity (the brain's ability to reorganise and form new neural connections), cognitive reserve (the accumulated resilience built through education, occupation, and mental engagement), and neuroprotection (the biological processes that defend neurons against damage from inflammation, oxidative stress, and toxic protein accumulation).
Unlike acute cognitive performance — which concerns how sharp you feel today — long-term brain health is about structural and functional preservation over decades. The hippocampus, prefrontal cortex, and white matter tracts that connect brain regions are all vulnerable to age-related changes, but the rate and severity of those changes vary enormously between individuals.7 Research increasingly shows that the choices you make in your 30s, 40s, and 50s significantly influence cognitive outcomes in your 70s and beyond.
A 2024 systematic review and meta-analysis examining life-course cognitive reserve found that early-life, mid-life, and late-life factors all independently contribute to dementia risk — education and occupational complexity in earlier decades, and social engagement and cognitive activity in later years.8
What Are the Biggest Modifiable Risk Factors for Cognitive Decline?
The 2024 Lancet Commission on dementia prevention identified 14 modifiable risk factors that together account for approximately 45% of all dementia cases globally.1 These risk factors operate across the life course, with different factors carrying more weight at different ages.
Early life (under 45): Low educational attainment is the dominant risk factor, reducing cognitive reserve — the brain's ability to compensate for age-related damage.
Mid-life (45–65): Hearing loss, hypertension, obesity, high LDL cholesterol, excessive alcohol consumption, traumatic brain injury, and physical inactivity all increase vulnerability. Hearing loss alone is the single largest modifiable risk factor, contributing an estimated 7% of attributable risk.1
Later life (65+): Smoking, depression, social isolation, diabetes, air pollution, and untreated vision loss become increasingly significant.
Two risk factors were newly added in the 2024 update: untreated vision loss and high LDL cholesterol. Both had sufficient evidence from longitudinal studies to meet the Commission's threshold for inclusion.1
The practical implication is profound: addressing even a subset of these factors — managing blood pressure, treating hearing and vision loss, maintaining physical activity, staying socially connected — can meaningfully reduce your lifetime risk of cognitive decline.
| Life Stage | Key Risk Factors | Mechanism of Harm |
|---|---|---|
| Early life (<45) | Low education | Reduced cognitive reserve |
| Mid-life (45–65) | Hearing loss, hypertension, obesity, high LDL cholesterol, excess alcohol, TBI, physical inactivity | Vascular damage, neuroinflammation, reduced neuroplasticity |
| Late life (65+) | Smoking, depression, social isolation, diabetes, air pollution, vision loss | Oxidative stress, neurodegeneration, reduced social stimulation |
How Does Physical Exercise Protect the Brain?
Physical exercise is one of the most consistently supported interventions for long-term brain health. Aerobic activity increases circulating levels of brain-derived neurotrophic factor (BDNF), a protein that promotes neurogenesis (the birth of new neurons) and synaptogenesis (the formation of new synaptic connections), particularly in the hippocampus — the brain's primary memory-processing region.2
Exercise also enhances cerebrovascular function, increasing blood flow and oxygen delivery to the brain. This is critical because the brain consumes approximately 20% of the body's oxygen despite representing only 2% of body mass. Improved vascular health reduces the risk of small vessel disease, a leading contributor to vascular dementia.
A 2025 review in The Lancet confirmed that exercise exerts neuroprotective effects through multiple pathways: neurotrophic signalling (BDNF, IGF-1, VEGF), neuroendocrine regulation, epigenetic modifications, and metabolic pathway optimisation.2 High-intensity interval training has demonstrated particular benefits for global cognition, attention, and verbal fluency in older adults with mild cognitive impairment.9
The evidence supports both aerobic exercise (walking, cycling, swimming) and resistance training. A 2025 narrative review found that combined aerobic and resistance training produced broader cognitive benefits than either modality alone, likely because they activate complementary neuroprotective mechanisms.9
How much exercise is enough? Current evidence supports at least 150 minutes of moderate-intensity aerobic activity per week, consistent with WHO guidelines. The cognitive benefits appear to follow a dose-response pattern — more activity generally yields greater protection — though even modest increases from a sedentary baseline offer meaningful benefit.
Why Is Sleep Essential for Long-Term Brain Health?
Sleep is when the brain performs critical maintenance. The glymphatic system — a waste-clearance network that operates primarily during deep slow-wave sleep — removes neurotoxic metabolites including amyloid-beta and tau proteins, both of which accumulate in Alzheimer's disease.3
During natural sleep, the interstitial space in the brain expands by up to 60%, significantly enhancing glymphatic flow and the clearance of these harmful proteins.3 A 2026 randomised crossover trial demonstrated that in human participants, glymphatic clearance during normal sleep increased morning plasma levels of Alzheimer's disease biomarkers compared to sleep deprivation — providing direct evidence that sleep actively flushes amyloid-beta from brain to blood.10
Sleep deprivation does not merely cause next-day fogginess. Chronic sleep disruption impairs memory consolidation (the process by which short-term memories become long-term ones), reduces glymphatic clearance, and may accelerate the accumulation of neurodegenerative pathology years or even decades before clinical symptoms appear.3
A bidirectional relationship exists: poor sleep increases neurotoxin accumulation, and neurotoxin accumulation further disrupts sleep — creating a self-reinforcing cycle that may begin in mid-life.11
What supports healthy sleep for brain health? Evidence-based approaches include maintaining consistent sleep-wake schedules, cognitive behavioural therapy for insomnia (CBT-I), circadian rhythm entrainment through morning light exposure, and addressing sleep disorders such as obstructive sleep apnoea, which independently increases dementia risk.
How Does Nutrition Influence Brain Ageing?
Dietary patterns have a direct and measurable impact on cognitive trajectories. The Mediterranean diet — characterised by high consumption of fruits, vegetables, whole grains, fish, legumes, and olive oil — has been the most extensively studied. A 2024 meta-analysis published in GeroScience found that higher adherence to the Mediterranean diet was associated with reduced risk of cognitive impairment, dementia, and Alzheimer's disease across multiple cohort studies.4
The MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay) specifically targets brain health by emphasising green leafy vegetables, berries, nuts, whole grains, fish, and olive oil whilst limiting red meat, butter, cheese, pastries, and fried food. A 2024 systematic review of 39 studies from 14 countries found that higher MIND diet adherence was protective against dementia in 7 of 10 cohorts, with positive associations for global cognition in 3 of 4 cohorts and episodic memory in 4 of 6 cohorts.12
The neuroprotective mechanisms involve multiple pathways. Polyphenols from berries and olive oil reduce neuroinflammation. Omega-3 fatty acids from oily fish support neuronal membrane integrity and anti-inflammatory signalling. B vitamins (particularly B6, B12, and folate) regulate homocysteine metabolism — elevated homocysteine is an independent risk factor for cognitive decline. Magnesium supports synaptic plasticity and neurotransmitter function. Antioxidants from colourful fruits and vegetables neutralise reactive oxygen species that damage neuronal DNA and cell membranes.
The evidence is more nuanced than headlines suggest. Whilst observational studies consistently show dietary associations, interventional trials have produced mixed results — the MIND diet's protective effect on cognitive decline appeared in 7 of 10 longitudinal cohorts but was less consistent in shorter-term interventional studies.12 This likely reflects the fact that dietary neuroprotection operates over decades, not weeks.
Can Nutritional Supplements Support Long-Term Brain Health?
Specific nutrients have demonstrated neuroprotective potential in clinical research, though supplements work best as a complement to a brain-healthy diet, not a replacement for one.
Omega-3 fatty acids (DHA and EPA) are among the most studied nutrients for brain health. DHA is a major structural component of neuronal cell membranes and supports synaptic function. A 2025 systematic review and dose-response meta-analysis of 58 studies found that omega-3 supplementation produced significant improvements in attention, perceptual speed, and language, with benefits becoming statistically significant at approximately 2,000 mg/day.6 However, the evidence is population-dependent: a 2024 systematic review found that omega-3 supplementation shows cognitive benefits in individuals with mild cognitive impairment or early Alzheimer's disease, but not in those with advanced dementia.13
Curcumin — the bioactive compound in turmeric — has shown promise as a neuroprotective agent, though curcumin's poor natural bioavailability and low solubility limit its ability to reach the brain. Specialized bioavailable formulations (such as liposomal or nano-particle delivery systems) address this limitation. A 2024 systematic review of 12 clinical studies found that these bioavailable curcumin formulations significantly improved cognitive performance (working memory, verbal fluency, and executive function) and reduced neuroinflammatory biomarkers including IL-6, TNF-α, and beta-amyloid in diverse adult populations.14
B vitamins play a critical role in homocysteine metabolism. The VITACOG trial (Smith et al., 2010) demonstrated that high-dose B vitamin supplementation (folic acid, B6, B12) slowed the rate of brain atrophy by 30% over two years specifically in older adults with elevated homocysteine (>13 µmol/L), with the greatest effect in those with the highest baseline levels.15 This suggests B vitamin supplementation may be particularly beneficial when homocysteine is elevated, rather than universally beneficial for all people with cognitive impairment.
Magnesium — particularly magnesium L-threonate, which crosses the blood-brain barrier more effectively than other forms — has been linked to improved synaptic density and cognitive function. A 2023 study using UK Biobank data from over 6,000 participants found that higher dietary magnesium intake was associated with larger brain volumes, particularly in women.16
| Nutrient | Key Evidence | Mechanism | Practical Note |
|---|---|---|---|
| Omega-3 (DHA/EPA) | 2025 meta-analysis: significant cognitive benefits at ≥2,000 mg/day6 | Membrane integrity, anti-inflammatory signalling | Benefits strongest in early cognitive decline, not advanced dementia |
| Curcumin | 2024 review: improved working memory, reduced neuroinflammatory markers14 | Anti-inflammatory, antioxidant, amyloid reduction | Bioavailability varies widely — formulation matters |
| B vitamins (B6, B12, folate) | VITACOG trial: 30% reduction in brain atrophy with elevated homocysteine15 | Homocysteine metabolism | Most benefit when homocysteine is elevated |
| Magnesium | UK Biobank: higher intake linked to larger brain volumes16 | Synaptic plasticity, neurotransmitter regulation | L-threonate form has superior CNS penetration |
It is important to note that no supplement alone can substitute for the combined effects of regular exercise, quality sleep, a nutrient-dense diet, and social engagement. Supplementation is most appropriately viewed as one component within a comprehensive brain health strategy.
How Do Stress and Social Connection Affect Your Brain?
Chronic psychological stress triggers sustained activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in prolonged cortisol elevation. Excessive cortisol exposure causes neuronal damage in the hippocampus — the brain region most critical for memory formation — through excitotoxicity, oxidative stress, and suppression of BDNF production.17
The consequences are measurable. Research shows that elderly individuals reporting increased stress are nearly three times more likely to develop Alzheimer's disease and demonstrate faster cognitive decline than those reporting low stress levels.17 A 2024 study in Translational Psychiatry identified that cortisol dysregulation, neuroinflammation, and cerebrovascular dysfunction form a linked biological triad in memory clinic patients, from subjective cognitive decline through to Alzheimer's disease.18
Social connection provides a powerful counterbalance. A 2024 meta-analysis combining data from 21 longitudinal studies and over 608,000 participants found that loneliness significantly increased the risk of all-cause dementia (HR 1.31), Alzheimer's disease (HR 1.39), and vascular dementia (HR 1.74) — even after controlling for depression, social isolation, and other modifiable risk factors.5
Conversely, active social participation in midlife and late life is associated with 30–50% lower subsequent dementia risk.19 Social engagement is thought to build and maintain cognitive reserve — the brain's accumulated resilience against pathological damage — by continuously stimulating complex cognitive processes including language, emotional processing, and executive function.
Practical stress-management approaches supported by evidence include regular physical activity (which directly lowers cortisol), mindfulness-based stress reduction, adequate sleep, and maintaining close social relationships. The 2024 Lancet Commission included social isolation as one of its 14 modifiable risk factors for dementia — underscoring that social health is brain health.1
What Does an Evidence-Based Brain Health Plan Look Like?
Protecting your brain is not about a single intervention — it requires a multi-domain approach that addresses the major modifiable risk factors identified by the Lancet Commission. Based on the current evidence, an effective brain health strategy includes:
Physical activity: At least 150 minutes per week of moderate-intensity aerobic exercise, ideally combined with resistance training two or more times per week. Walking, cycling, swimming, and dancing all qualify.
Sleep optimisation: Prioritise 7–9 hours of quality sleep nightly. Maintain consistent sleep-wake times. Address sleep disorders — particularly obstructive sleep apnoea — promptly, as untreated sleep apnoea independently increases dementia risk.
Brain-healthy nutrition: Follow a Mediterranean or MIND dietary pattern emphasising vegetables, berries, oily fish, nuts, whole grains, and olive oil. Minimise ultra-processed food, excessive sugar, and saturated fat.
Cognitive engagement: Continue learning throughout life. Education, occupational complexity, reading, language learning, and novel cognitive challenges all contribute to cognitive reserve.
Social connection: Maintain and nurture close relationships. Participate in group activities. Address loneliness proactively — it is a biological risk factor, not merely a quality-of-life issue.
Stress management: Regular physical activity, mindfulness practices, adequate sleep, and strong social bonds all help regulate the HPA axis and reduce chronic cortisol exposure.
Medical management: Control blood pressure, manage diabetes, treat hearing and vision loss, monitor cholesterol. These medical factors are directly included in the Lancet Commission's modifiable risk list.
Targeted nutritional support: Where dietary gaps exist, consider evidence-based supplements — omega-3 fatty acids, B vitamins (particularly if homocysteine is elevated), magnesium, and curcumin — as a complement to dietary and lifestyle strategies.
This is not about perfection. Each of these factors contributes independently, and addressing even a few meaningfully reduces lifetime risk. The evidence suggests that starting earlier yields greater protection, but improvements at any age offer benefit.
Frequently Asked Questions
At what age should you start thinking about long-term brain health?
Brain health is a lifespan concern, not just a later-life priority. The 2024 Lancet Commission's life-course model identifies modifiable risk factors from early adulthood onward — including educational attainment, physical activity, and cardiovascular health.1 Research on cognitive reserve suggests that the resilience your brain builds in your 20s, 30s, and 40s directly influences your vulnerability to decline decades later.8 Starting earlier provides more time to accumulate neuroprotective benefits, though improvements at any age are worthwhile.
Can you reverse cognitive decline that has already started?
The evidence depends on the stage and cause. Lifestyle interventions — particularly exercise, sleep improvement, and dietary changes — have demonstrated cognitive improvements in people with mild cognitive impairment (MCI). Omega-3 supplementation shows benefits in early cognitive decline but not in advanced dementia.13 Addressing reversible causes such as depression, sleep disorders, B12 deficiency, or medication side effects can also restore function. However, once significant neurodegeneration has occurred (as in moderate-to-advanced Alzheimer's disease), recovery of lost function is limited with current interventions.
How much does genetics influence brain health compared to lifestyle?
The 2024 Lancet Commission estimated that modifiable risk factors account for approximately 45% of all dementia cases.1 While genetic factors — including APOE4 carrier status — influence individual risk, they do not determine outcomes. Even APOE4 carriers benefit significantly from lifestyle modification. The majority of cognitive ageing is shaped by the interaction between genetic predisposition and modifiable environmental, behavioural, and nutritional factors.
Is brain training effective for preventing cognitive decline?
Structured cognitive training can improve specific cognitive abilities, but the evidence for broad transfer (improvement in untrained domains) is limited. The ACTIVE trial found that certain forms of cognitive training — particularly speed-of-processing training — produced benefits lasting up to 10 years.20 However, passive activities like crossword puzzles or brain-game apps have less robust evidence. The most protective form of cognitive engagement appears to be sustained learning of complex new skills — such as learning a musical instrument or a new language.
Does hearing loss really affect brain health?
Hearing loss is the single largest modifiable risk factor for dementia, contributing an estimated 7% of attributable risk according to the 2024 Lancet Commission.1 The mechanisms include reduced cognitive stimulation, increased cognitive load (the brain works harder to decode degraded auditory signals), and social withdrawal. The ACHIEVE trial (2023) found that hearing intervention reduced cognitive decline by 48% over three years, but only in a subgroup of older adults at particularly high risk — those recruited from a cardiovascular health study with more comorbidities (n=238). In a separately recruited general healthy volunteer subgroup (n=739), hearing aids showed no significant cognitive benefit within the 3-year timeframe.21 This suggests that hearing intervention may be particularly beneficial for those with multiple dementia risk factors, though longer-term studies are needed to confirm benefits in the general population. Treating hearing loss is still one of the most impactful single interventions for brain health, particularly for individuals with elevated risk.
What is the difference between normal age-related changes and concerning decline?
Normal ageing involves gradual slowing of processing speed, occasional difficulty retrieving names, and mild reduction in multitasking ability. These changes do not significantly impair daily functioning. Concerning signs include consistently forgetting recent events, difficulty following familiar routes, problems managing finances, personality changes, and impaired judgement. The distinction matters because normal changes do not progress to dementia in most people, whilst MCI carries a conversion rate of approximately 10–15% per year to dementia.
Supporting Your Cognitive Health with BrainSmart
Long-term brain health depends on the interplay of lifestyle factors and nutritional support. Ensuring your brain receives adequate levels of key nutrients — including omega-3 fatty acids, B vitamins, magnesium, and antioxidants — is an important component of a comprehensive cognitive health strategy.
Explore our range of evidence-based brain health supplements: BrainSmart Ultra for comprehensive brain support, BrainSmart Focus for concentration and mental clarity, BrainSmart Memory for memory and recall, and BrainSmart Mood for emotional wellbeing and stress.
Related Reading
Explore more evidence-based guides from the BrainSmart Knowledge Centre to deepen your understanding of brain health.
- The Complete Guide to Cognitive Performance
Covers the acute performance side of brain health — focus, mental clarity, and processing speed — complementing this guide's long-term perspective.
- Memory and Learning: How Your Brain Stores, Retrieves, and Strengthens Information
A deep dive into the memory systems referenced throughout this guide, including hippocampal function and memory consolidation during sleep.
- Mood, Stress, and Your Brain: A Comprehensive Guide to Emotional Wellbeing
Explores the stress–brain connection in greater depth, including HPA axis regulation and serotonin pathways discussed in this article.
- Omega-3 Fatty Acids and Brain Health: DHA, EPA, and Beyond
Detailed evidence review of the omega-3 research summarised in this guide, including dosage guidance and population-specific findings.
- Brain Health After 50: Evidence-Based Strategies for Cognitive Longevity
Applies the life-course framework discussed here to the specific challenges and opportunities of cognitive health in later life.
- Neuroplasticity: How Your Brain Adapts and Why It Matters at Every Age
Explores the neuroplasticity mechanisms underlying cognitive reserve — a central concept in long-term brain protection.
- Anti-Inflammatory Nutrients and Neuroprotection
A detailed look at the anti-inflammatory pathways discussed in this guide, including curcumin, polyphenols, and omega-3 mechanisms.
- The Best Foods for Brain Health: A Nutrient-by-Nutrient Breakdown
Practical nutrition guidance that expands on the Mediterranean and MIND diet evidence presented here.
- Magnesium and the Brain: Why Deficiency Affects Mood, Sleep, and Cognition
Explores the magnesium research referenced in this guide, including L-threonate bioavailability and UK Biobank findings.
- Brain Fog: Causes, Science, and Evidence-Based Solutions
Covers the symptoms and mechanisms that often serve as early warning signs of the long-term risks discussed in this guide.
Author
Tom Kaplan
Brain Health Writer at BrainSmart
Tom Kaplan is a specialist health writer focused on cognitive health, brain nutrition, and evidence-based approaches to supporting mental performance across the lifespan. His work draws on peer-reviewed research across neuroscience, nutritional psychiatry, and cognitive psychology — translating complex clinical findings into clear, practical guidance that helps readers make informed decisions about their brain health. Read Full Bio →
References
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