Here's something worth sitting with: long-term brain health isn't just about avoiding disease. It's the sustained preservation of everything that makes you you — your memory, reasoning, attention, and processing speed — across your entire lifespan. It encompasses the biological, nutritional, and lifestyle factors that determine whether your brain stays resilient as you age or gradually becomes vulnerable to decline.
And the evidence here is genuinely encouraging: 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 Think about that for a moment — nearly half of dementia risk is within your influence, shaped by 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 people.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?
When we talk about long-term brain health, we're really talking about your brain's capacity to keep doing what it does best — learning, remembering, regulating emotions, and making sound decisions — throughout your entire life. That capacity 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 here's what's really interesting: 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.
This is where it gets genuinely empowering. 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 The takeaway? Your brain's trajectory is shaped continuously, not fixed at any single moment.
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 — and that pattern itself is worth paying attention to.
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): This is where the list gets surprisingly long. 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
What this means for you is actually quite 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?
If there's one intervention that keeps showing up across virtually every area of brain health research, it's physical exercise. 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, boosting blood flow and oxygen delivery to your brain. That matters because the brain consumes approximately 20% of the body's oxygen despite representing only 2% of body mass — it's a remarkably hungry organ with little tolerance for under-supply. Improved vascular health reduces your risk of small vessel disease, a leading contributor to vascular dementia.
A 2025 review in The Lancet confirmed that exercise protects the brain through multiple pathways at once: neurotrophic signalling (BDNF, IGF-1, VEGF), neuroendocrine regulation, epigenetic modifications, and metabolic pathway optimisation.2 High-intensity interval training, in particular, has demonstrated meaningful 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 combining the two 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. And here's the encouraging part: you don't need to train like an athlete. Walking briskly, cycling to work, or swimming a few times a week is enough to begin producing measurable changes in brain function.
Why Is Sleep Essential for Long-Term Brain Health?
Sleep isn't just rest — it's when your brain performs some of its most critical maintenance work. 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
This is where the biology gets fascinating. 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 In practical terms: the sleep you get in your 40s and 50s helps shape the brain you carry into your 70s.
There's also a troubling feedback loop at work here: 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 times, 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. If you've been treating poor sleep as a productivity issue rather than a health one, the evidence strongly suggests it deserves higher priority.
How Does Nutrition Influence Brain Ageing?
What you eat has a direct and measurable impact on how your brain ages. Of all the dietary patterns studied, the Mediterranean diet — characterised by high consumption of fruits, vegetables, whole grains, fish, legumes, and olive oil — has received the most extensive attention. A 2025 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) takes this a step further by specifically targeting brain health. It emphasises green leafy vegetables, berries, nuts, whole grains, fish, and olive oil whilst limiting red meat, butter, cheese, pastries, and fried food. A 2025 systematic review of 39 studies from 14 countries found that higher MIND diet adherence was associated with reduced dementia and Alzheimer's risk in most longitudinal cohorts and with better global cognition and episodic memory in 4 of 6 cohorts.12
So how does this translate at the cellular level? Several pathways operate in parallel, and each one is worth understanding. 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.
That said, the evidence is more nuanced than headlines often 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. What this means for your daily choices: consistency over years matters far more than any single meal, and small sustained shifts genuinely compound over time.
Can Nutritional Supplements Support Long-Term Brain Health?
Specific nutrients have demonstrated real neuroprotective potential in clinical research — though it's worth being upfront: 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, and for good reason. 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 At this dose level, omega-3s may increase bleeding risk in individuals taking anticoagulant or antiplatelet medications — discuss with your healthcare provider before supplementing at higher doses. 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 genuine promise as a neuroprotective agent, though there's an important caveat: 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. Recent reviews of bioavailable curcumin formulations report improvements in inflammatory markers and modest cognitive benefits in some adult populations, although the evidence base is smaller and less consistent than for omega-3 fatty acids. A 2018 double-blind RCT (Small et al., Am J Geriatr Psychiatry) found that a bioavailable curcumin formulation improved memory and attention over 18 months in non-demented adults, with corresponding reductions in amyloid and tau PET signals.14
B vitamins play a critical role in homocysteine metabolism, and the evidence here is particularly compelling. 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 approximately 30% over two years in older adults with mild cognitive impairment, with substantially larger reductions (around 50%) in the subgroup with elevated homocysteine (>13 µmol/L).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 | Small 2018 RCT: improved memory/attention, reduced amyloid/tau signals14 | 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's worth emphasising: no supplement alone can substitute for the combined effects of regular exercise, quality sleep, a nutrient-dense diet, and social engagement. Before adding a new supplement — particularly if you are taking prescription medication, have a chronic health condition, or are over 65 — discuss it with your GP or pharmacist, as some supplements interact with common medications. Supplementation is best understood as one component within a comprehensive brain health strategy — a useful complement where dietary gaps exist, but never a substitute for the foundations.
How Do Stress and Social Connection Affect Your Brain?
Chronic psychological stress does something remarkably specific to your brain. It 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 older adults reporting elevated stress are approximately twice as likely to develop Alzheimer's disease and to demonstrate faster cognitive decline than those reporting low stress.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
Now here's something that might surprise you: social connection provides a remarkably 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 appears 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.
So what can you actually do about it? The evidence supports a few practical levers: 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 really 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, here's what an effective brain health strategy looks like in practice:
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: Keep 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 genuinely offer benefit — so wherever you are right now is the right time to begin.
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 Genetic factors — including APOE4 carrier status — influence your individual risk, but they do not determine your outcome. Even APOE4 carriers benefit significantly from lifestyle modification. The majority of cognitive ageing is shaped by the interaction between genetic predisposition and the modifiable environmental, behavioural, and nutritional factors within your control.
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 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 — taking up a musical instrument, picking up a new language, or developing a serious creative practice all qualify.
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 you can pursue, particularly if you carry other dementia risk factors.
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 don't 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: normal changes do not progress to dementia in most people, whilst MCI carries a conversion rate of approximately 10–15% per year to dementia. If you're noticing patterns from the second list rather than the first, it's worth raising with your GP — early evaluation matters.
Supporting Long-Term Brain Health
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.
When choosing a supplement for long-term neuroprotection, look for formulations that include omega-3 DHA, homocysteine-lowering B vitamins, and magnesium at evidence-supported doses. BrainSmart's Ultra formulation is designed around these nutrients, and you can explore the full range here.
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
References
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- Tari AR, Walker TL, Bhatt D, et al. Neuroprotective mechanisms of exercise and the importance of fitness for healthy brain ageing. Lancet. 2025;405(10484):1093-1118. doi:10.1016/S0140-6736(25)00184-9
- van Hattem T, Verkaar L, Krugliakova E, et al. Targeting sleep physiology to modulate glymphatic brain clearance. Physiology. 2025;40(3). doi:10.1152/physiol.00019.2024
- Fekete M, Szarvas Z, Fazekas-Pongor V, et al. The role of the Mediterranean diet in reducing the risk of cognitive impairment, dementia, and Alzheimer's disease: a meta-analysis. GeroScience. 2025;47(3):3111-3130. doi:10.1007/s11357-024-01488-3
- Luchetti M, Terracciano A, Stephan Y, Sutin AR. A meta-analysis of loneliness and risk of dementia using longitudinal data from >600,000 individuals. Nature Mental Health. 2024;2:1453-1461. doi:10.1038/s44220-024-00328-9
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- Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. Lancet. 2017;390(10113):2673-2734. doi:10.1016/S0140-6736(17)31363-6
- Liu Y, Lu G, Liu L, He Y, Gong W. Cognitive reserve over the life course and risk of dementia: a systematic review and meta-analysis. Frontiers in Aging Neuroscience. 2024;16:1358992. doi:10.3389/fnagi.2024.1358992
- Ramirez-Campillo R, Castañeda-Babarro A, Calleja-González J, et al. Physical activity to counter age-related cognitive decline: benefits of aerobic, resistance, and combined training — a narrative review. Sports Medicine - Open. 2025;11(1). (Narrative review)
- Eide PK, Vinje V, Pripp AH, et al. The glymphatic system clears amyloid beta and tau from brain to plasma in humans. Nature Communications. 2026;17:715. doi:10.1038/s41467-026-68374-8
- Mander BA, Winer JR, Walker MP. Sleep and human aging. Neuron. 2017;94(1):19-36. doi:10.1016/j.neuron.2017.02.004
- Berendsen AAM, Kang JH, van de Rest O, et al. The association between the MIND diet and cognitive health in middle-aged and older adults: a systematic review. Revue Neurologique. 2025;181(7):652-665. doi:10.1016/j.neurol.2025.04.002
- Barros MI, Brandao T, Irving SC, et al. Omega-3 polyunsaturated fatty acids and cognitive decline in adults with non-dementia or mild cognitive impairment: an overview of systematic reviews. Nutrients. 2025;17(18):3002. doi:10.3390/nu17183002
- Small GW, Siddarth P, Li Z, et al. Memory and brain amyloid and tau effects of a bioavailable form of curcumin in non-demented adults: a double-blind, placebo-controlled 18-month trial. Am J Geriatr Psychiatry. 2018;26(3):266-277. doi:10.1016/j.jagp.2017.10.010
- Smith AD, Smith SM, de Jager CA, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS ONE. 2010;5(9):e12244. doi:10.1371/journal.pone.0012244
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- Ouanes S, Popp J. High cortisol and the risk of dementia and Alzheimer's disease: a review of the literature. Frontiers in Aging Neuroscience. 2019;11:43. doi:10.3389/fnagi.2019.00043
- Daniilidou M, Holleman J, Hagman G, et al. Neuroinflammation, cerebrovascular dysfunction and diurnal cortisol biomarkers in a memory clinic cohort: findings from the Co-STAR study. Translational Psychiatry. 2024;14:364. doi:10.1038/s41398-024-03072-x
- Sommerlad A, Kivimäki M, Larson EB, et al. Social participation and risk of developing dementia. Nature Aging. 2023;3(5):532-545. doi:10.1038/s43587-023-00387-0
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- Lin FR, Pike JR, Albert MS, et al. Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss in the USA (ACHIEVE): a multicentre, randomised controlled trial. Lancet. 2023;402(10404):786-797. doi:10.1016/S0140-6736(23)01406-X
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 →