TL;DR: Your ability to form, store, and retrieve memories is not fixed — it is shaped daily by what you eat. The hippocampus, the brain’s memory hub, requires a steady supply of choline (for acetylcholine synthesis), DHA (for synaptic membrane integrity), flavonoids (for BDNF upregulation and cerebral blood flow), B vitamins (to keep neurotoxic homocysteine in check), and curcumin (for anti-inflammatory and neurotrophic support). The MIND diet — a hybrid of Mediterranean and DASH patterns emphasizing berries, leafy greens, fish, nuts, and olive oil — has been associated with a 53% reduced risk of Alzheimer’s in observational studies and measurably slower cognitive decline. On the other side of the ledger, diets high in added sugar, ultra-processed foods, and excess alcohol actively damage hippocampal structure and suppress BDNF. Exercise amplifies every dietary intervention by driving BDNF to levels no food alone can match, and sleep is the non-negotiable period during which newly encoded memories are consolidated into long-term storage. A memory-optimizing diet is not exotic — it is a pattern of consistently eating whole, nutrient-dense foods while avoiding the modern dietary insults that erode the brain’s capacity to remember.

Introduction

Memory is among the cognitive functions people fear losing most — and among the most responsive to dietary intervention. Unlike processing speed, which declines relatively steadily with age, memory performance is surprisingly malleable. Decades of research have established that specific nutrients support the biological machinery of memory, while certain dietary patterns actively degrade it.

This is not a matter of marginal effects. The Nurses’ Health Study, tracking over 16,000 women for decades, found that those who consumed the most blueberries and strawberries delayed memory decline by up to 2.5 years compared to those who consumed the least (Devore et al., 2012, Annals of Neurology). The MIND diet trials have shown that strong adherence is associated with roughly half the risk of developing Alzheimer’s disease. These are not supplement studies with optimistic extrapolations — they are large-scale, long-duration investigations of ordinary dietary patterns producing extraordinary differences in brain aging.

To understand why food matters so much for memory, it helps to understand how memory works at a biological level — and where, precisely, nutrition intersects with the molecular processes of remembering.

How Memory Works

Encoding, Consolidation, and Retrieval

Memory is not a single event but a sequence of three distinct biological processes.

Encoding is the initial registration of information — the moment a sensory experience is converted into a neural representation. Encoding depends on attention (you cannot remember what you did not notice) and on the neurotransmitter acetylcholine, which modulates the signal-to-noise ratio in cortical circuits and gates which incoming information gets flagged as worth storing.

Consolidation is the process by which fragile, newly encoded memories are stabilized into durable, long-term storage. Consolidation occurs primarily during sleep — specifically during slow-wave sleep and REM sleep — when the hippocampus replays the day’s encoded experiences and transfers them to neocortical networks for permanent storage. This process requires BDNF (brain-derived neurotrophic factor) for the synaptic strengthening that underlies long-term potentiation, the cellular mechanism of durable memory.

Retrieval is the process of accessing stored memories when needed. Retrieval depends on the integrity of hippocampal-cortical circuits and on the neurotransmitter environment at the moment of recall. Stress hormones, particularly cortisol, can impair retrieval even when memories have been successfully encoded and consolidated — a fact familiar to anyone who has gone blank during an exam despite thorough preparation.

The Hippocampus: Memory’s Central Hub

The hippocampus — a seahorse-shaped structure in the medial temporal lobe — is the brain region most critical for the formation of new declarative memories (facts and events). Damage to the hippocampus, as in the famous case of patient H.M. studied by Brenda Milner, produces a devastating inability to form new memories while leaving older memories largely intact.

The hippocampus is also one of only two brain regions where adult neurogenesis — the birth of new neurons — continues throughout life. This ongoing neurogenesis, supported by BDNF, is believed to contribute to the hippocampus’s capacity for pattern separation (distinguishing between similar memories) and cognitive flexibility. Crucially, the hippocampus is exceptionally vulnerable to metabolic insult. It is among the first structures to atrophy in Alzheimer’s disease, among the most sensitive to elevated blood sugar and cortisol, and among the most responsive to dietary and exercise interventions.

This vulnerability is also an opportunity. If the hippocampus is the brain structure most easily damaged by poor diet, it is also the structure most readily protected and even restored by a good one.

Key Nutrients for Memory

Choline and Acetylcholine

Acetylcholine is the neurotransmitter most directly involved in memory encoding. The cholinergic system — projecting from the basal forebrain to the hippocampus and cortex — determines which incoming information receives the attentional stamp required for memory formation. This is not theoretical: every major Alzheimer’s drug approved in the twentieth century (donepezil, rivastigmine, galantamine) works by inhibiting acetylcholine breakdown, effectively boosting cholinergic signaling in a brain that is losing its cholinergic neurons.

Acetylcholine is synthesized from choline, an essential nutrient that must be obtained from the diet. The adequate intake is 550 mg per day for men and 425 mg for women, yet survey data consistently show that the vast majority of adults fall short. Poly et al. (2011), in a study from the Framingham Offspring Cohort published in the American Journal of Clinical Nutrition, found that higher concurrent choline intake was significantly associated with better verbal and visual memory performance and with reduced white-matter hyperintensity volume — a marker of cerebrovascular damage linked to cognitive decline.

The richest dietary sources of choline are egg yolks (approximately 147 mg per large egg), beef liver (356 mg per 3 oz), salmon (75 mg per 3 oz), soybeans (107 mg per cup), and cruciferous vegetables (modest amounts). Two to three eggs per day provide roughly half the daily choline requirement and represent one of the most efficient memory-supporting dietary habits available.

Omega-3 Fatty Acids and DHA

Docosahexaenoic acid (DHA), the dominant omega-3 fatty acid in brain tissue, constitutes approximately 40% of the polyunsaturated fatty acids in neuronal membranes. DHA maintains the fluidity and functional integrity of synaptic membranes, which is essential for the rapid neurotransmitter signaling that underlies memory encoding and retrieval.

Beyond its structural role, DHA directly supports BDNF expression. Wu et al. (2004), in Neuroscience, demonstrated that dietary DHA supplementation increased hippocampal BDNF levels in animal models, while DHA deficiency reduced BDNF and impaired spatial learning. In humans, Yurko-Mauro et al. (2010), in a randomized controlled trial published in Alzheimer’s & Dementia, found that 900 mg of DHA daily for 24 weeks significantly improved episodic memory in healthy older adults with age-related cognitive complaints. The improvement was equivalent to having the learning and memory skills of someone approximately three years younger.

Fatty fish — salmon, mackerel, sardines, herring, and anchovies — are the most bioavailable dietary sources of DHA. Two to three servings per week provides approximately 500-1,000 mg of combined EPA and DHA, consistent with the intake levels associated with cognitive benefits in epidemiological studies.

Flavonoids and Blueberries

Flavonoids — a broad class of polyphenolic compounds found in berries, tea, cocoa, and colorful fruits and vegetables — have emerged as among the most promising dietary compounds for memory preservation. Their effects operate through multiple mechanisms: increasing BDNF expression, enhancing cerebral blood flow, reducing neuroinflammation, and directly modulating synaptic plasticity signaling pathways.

The most compelling human evidence comes from the Nurses’ Health Study. Devore et al. (2012), analyzing data from 16,010 women aged 70 and older in Annals of Neurology, found that greater intake of blueberries and strawberries was associated with slower rates of cognitive decline. Women with the highest berry intake showed memory performance equivalent to women 2.5 years younger than those with the lowest intake. The association remained significant after adjustment for overall diet quality, socioeconomic status, physical activity, and other confounders.

Krikorian et al. (2010), in a randomized controlled trial published in the Journal of Agricultural and Food Chemistry, demonstrated that 12 weeks of daily wild blueberry juice consumption improved paired associate learning and word list recall in older adults with early memory decline compared to a placebo beverage. More recently, a larger RCT by Bowtell et al. (2017), published in Applied Physiology, Nutrition, and Metabolism, showed that blueberry concentrate supplementation for 12 weeks increased brain activation in regions associated with working memory during fMRI tasks.

Anthocyanins — the pigments responsible for the blue, purple, and deep red colors in berries — are the flavonoid subclass most consistently linked to memory benefits. They cross the blood-brain barrier and accumulate in the hippocampus and cortex, where they influence signaling pathways including CREB and ERK that are essential for long-term potentiation.

Curcumin

Curcumin, the principal bioactive compound in turmeric, has demonstrated memory-enhancing effects through both anti-inflammatory and neurotrophic mechanisms. Small et al. (2018), in an 18-month randomized, double-blind, placebo-controlled trial published in The American Journal of Geriatric Psychiatry, found that a bioavailable curcumin formulation (Theracurmin, 90 mg twice daily) significantly improved memory performance and attention in non-demented older adults. Remarkably, PET neuroimaging revealed that the curcumin group had significantly lower amyloid and tau accumulation in brain regions critical for memory — the amygdala and hypothalamus — compared to placebo.

The anti-inflammatory mechanism is particularly relevant for memory. Chronic low-grade neuroinflammation — driven by aging, poor diet, and metabolic dysfunction — impairs hippocampal neurogenesis and suppresses BDNF. Curcumin is among the most potent natural inhibitors of NF-kB, the master transcription factor for inflammatory signaling.

Bioavailability remains the practical challenge. Standard turmeric powder delivers negligible curcumin to the bloodstream. Consuming turmeric with black pepper (which contains piperine, an absorption enhancer) and fat (curcumin is lipophilic) improves uptake meaningfully. Bioavailable supplement formulations are an alternative for those seeking the doses used in clinical trials.

B Vitamins and Homocysteine

Elevated homocysteine — an amino acid metabolite that accumulates when B vitamin status is inadequate — is an established risk factor for cognitive decline and hippocampal atrophy. Homocysteine is neurotoxic: it promotes oxidative stress, damages cerebrovascular endothelium, and directly impairs synaptic plasticity.

The VITACOG trial (Smith et al., 2010, PLOS ONE) provided some of the most striking evidence linking B vitamins to memory preservation. In this randomized, double-blind, placebo-controlled trial of 168 older adults with mild cognitive impairment, high-dose B vitamin supplementation (folate 800 mcg, B12 500 mcg, B6 20 mg) for two years reduced the rate of brain atrophy by 30% compared to placebo. In a subsequent analysis, de Jager et al. (2012, International Journal of Geriatric Psychiatry) demonstrated that the B vitamin group showed significantly less decline in episodic memory and semantic memory over the trial period. The protective effect was most pronounced in participants with elevated baseline homocysteine — precisely the group in which B vitamin supplementation lowered homocysteine most effectively.

Dietary sources of the relevant B vitamins include leafy greens and legumes (folate), meat, fish, eggs, and dairy (B12), and poultry, fish, potatoes, and bananas (B6). Vegans are at particular risk of B12 deficiency and should supplement.

The MIND Diet and Memory

The MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay), developed by Martha Clare Morris and colleagues at Rush University, was specifically designed to incorporate the dietary components with the strongest evidence for neuroprotection. It is not a generic healthy-eating plan — it was engineered by analyzing which specific foods and nutrients were most consistently associated with reduced cognitive decline across epidemiological studies.

The MIND diet emphasizes ten brain-healthy food groups: leafy green vegetables (at least six servings per week), other vegetables, nuts (five servings per week), berries (especially blueberries, at least two servings per week), beans, whole grains, fish (at least once per week), poultry, olive oil (as the primary cooking fat), and wine (one glass per day, optional). It limits five food groups: red meat, butter and margarine, cheese, pastries and sweets, and fried and fast food.

Morris et al. (2015), in a prospective study of 923 older adults published in Alzheimer’s & Dementia, found that high adherence to the MIND diet was associated with a 53% reduction in Alzheimer’s disease risk over 4.5 years of follow-up. Even moderate adherence — following the diet imperfectly but consistently — was associated with a 35% risk reduction. The MIND diet outperformed both the Mediterranean and DASH diets individually for cognitive outcomes, suggesting that its specific emphasis on berries, leafy greens, and fish captures uniquely brain-relevant dietary components.

A follow-up analysis by Morris et al. (2015), published in Alzheimer’s & Dementia, found that MIND diet adherence was associated with significantly slower decline in global cognitive function, with the difference between the highest and lowest tertiles of adherence equivalent to being 7.5 years younger cognitively. The effects were strongest for episodic memory — the type of memory most dependent on hippocampal function.

It is important to note that the large randomized controlled trial of the MIND diet (the MIND Diet Trial, published in 2023 in The New England Journal of Medicine) did not show a statistically significant cognitive benefit over a control diet with mild caloric restriction over three years in cognitively healthy adults. However, the control group also improved, baseline cognitive impairment was minimal, and the study population may have been too healthy to demonstrate dietary effects within the trial period. The observational evidence across multiple large cohorts remains compelling, and the MIND diet’s component foods align with the mechanistic evidence reviewed throughout this article.

Foods That Impair Memory

Added Sugar and High-Glycemic Diets

The hippocampus is exquisitely sensitive to glucose dysregulation. Molteni et al. (2002), in Neuroscience, showed that a high-sucrose diet reduced hippocampal BDNF levels and impaired spatial learning in rats within just two months. In humans, Kerti et al. (2013), in a study published in Neurology, found that higher blood glucose levels — even within the normal, non-diabetic range — were associated with smaller hippocampal volume and poorer memory performance in older adults. The relationship was linear: every increment in average blood sugar corresponded to a decrement in hippocampal size and memory function.

The mechanism involves multiple pathways. Chronic hyperglycemia promotes the formation of advanced glycation end-products (AGEs), which damage neuronal proteins and membranes. Insulin resistance reduces the brain’s ability to utilize glucose efficiently and impairs insulin-dependent signaling in the hippocampus — signaling that is directly involved in memory consolidation. Elevated blood sugar also suppresses BDNF, reducing the neurotrophic support the hippocampus requires for ongoing neurogenesis and synaptic maintenance.

Practical implication: minimizing added sugar and refined carbohydrates is one of the highest-yield dietary strategies for memory preservation.

Ultra-Processed Foods

Ultra-processed foods (UPFs) — industrially formulated products typically high in refined sugars, seed oils, emulsifiers, and artificial additives — have been linked to accelerated cognitive decline in multiple large prospective studies. Goncalves et al. (2023), in a study from the NutriNet-Sante cohort published in JAMA Neurology, found that higher ultra-processed food consumption was associated with faster rates of global cognitive decline and executive function decline over a median follow-up of eight years.

The damage extends beyond the sugar and fat content. UPFs alter the gut microbiome in ways that increase systemic inflammation, reduce short-chain fatty acid production (butyrate independently supports hippocampal BDNF), and disrupt the gut-brain axis. The displacement effect compounds the problem: every meal built around ultra-processed foods is a meal that excludes the polyphenol-rich, omega-3-rich, and fiber-rich whole foods that actively support memory.

Excess Alcohol

Moderate alcohol consumption (one drink per day for women, up to two for men) has a complex and contested relationship with cognitive health. However, the evidence is unambiguous that heavy and chronic alcohol consumption is toxic to memory systems. Alcohol directly damages the hippocampus, impairs neurogenesis, depletes B vitamins (particularly thiamine, whose deficiency causes the devastating amnesia of Wernicke-Korsakoff syndrome), and disrupts sleep architecture — specifically the slow-wave and REM sleep stages during which memory consolidation occurs.

Topiwala et al. (2017), in a large observational study published in the BMJ, found that even moderate alcohol consumption (14-21 units per week) was associated with hippocampal atrophy in a dose-dependent manner. The right hippocampus — particularly important for spatial and contextual memory — was most affected. There was no level of alcohol consumption that was associated with a benefit to hippocampal volume.

For memory optimization, the most prudent approach is either abstaining or limiting alcohol to modest, occasional consumption — and never using alcohol as a sleep aid, as it fragments the very sleep stages memory consolidation requires.

Exercise as a Memory Amplifier

No dietary intervention matches the magnitude of memory benefit produced by regular aerobic exercise. Exercise is the single most potent stimulus for hippocampal BDNF production, hippocampal neurogenesis, and hippocampal volume preservation — the three biological processes most directly linked to memory function.

Erickson et al. (2011), in a landmark randomized controlled trial published in Proceedings of the National Academy of Sciences, demonstrated that one year of moderate aerobic exercise (walking 40 minutes, three times per week) increased hippocampal volume by 2% in older adults — effectively reversing one to two years of age-related hippocampal atrophy. The hippocampal volume increase was accompanied by elevated serum BDNF and significant improvements in spatial memory. The stretching-and-toning control group showed the expected age-related hippocampal decline over the same period.

Exercise amplifies dietary interventions through converging mechanisms. It increases cerebral blood flow (improving nutrient delivery to the brain), upregulates BDNF (potentiating the effects of dietary BDNF supporters like flavonoids and DHA), enhances insulin sensitivity (reversing the glucose dysregulation that damages the hippocampus), and improves sleep quality (which is essential for memory consolidation). Van Praag et al. (2007), in the Journal of Neuroscience, demonstrated that the combination of exercise and a flavonoid-enriched diet produced greater hippocampal neurogenesis and better memory performance than either intervention alone.

The minimum effective dose for memory benefits appears to be 150 minutes per week of moderate-intensity aerobic exercise — brisk walking, cycling, swimming, or dancing. The evidence suggests that this is not a ceiling but a floor: more exercise, within reason, produces greater benefits.

Sleep and Memory Consolidation

Sleep is not merely restorative for the brain — it is the period during which memory consolidation actively occurs. Without adequate sleep, encoding may proceed normally, but the transfer of memories from short-term hippocampal storage to long-term neocortical storage is fundamentally impaired.

Walker and Stickgold (2006), in a review published in Neuron, described the two-stage model of memory consolidation during sleep. During slow-wave sleep (predominant in the first half of the night), the hippocampus replays encoded experiences and transfers them to cortical networks. During REM sleep (predominant in the second half), these newly transferred memories are integrated with existing knowledge and stabilized. Disrupting either stage impairs memory — slow-wave sleep disruption particularly impairs declarative (factual) memory, while REM disruption impairs procedural and emotional memory.

Mander et al. (2013), in a study published in Nature Neuroscience, demonstrated that the age-related decline in slow-wave sleep directly predicted the degree of overnight memory impairment in older adults and that this effect was mediated by prefrontal cortex atrophy. Sleep quality is not a peripheral concern for memory — it is a central mechanism.

Dietary factors that support sleep quality — magnesium (which promotes GABA-mediated relaxation), tryptophan-containing foods (which support serotonin and melatonin synthesis), and avoidance of caffeine in the afternoon and evening — are therefore indirectly but meaningfully supportive of memory consolidation.

Practical Takeaway

Memory is a biological process with specific nutritional inputs. The following evidence-based strategies provide a framework for a memory-optimizing diet:

  1. Eat choline-rich foods daily. Two to three eggs per day, regular consumption of fish or soy, or supplementation with alpha-GPC or citicoline ensures adequate substrate for acetylcholine synthesis — the neurotransmitter most directly involved in memory encoding. Most adults are deficient.

  2. Consume fatty fish at least twice per week. Salmon, mackerel, sardines, and herring provide the DHA that maintains synaptic membrane integrity and drives hippocampal BDNF expression. If you do not eat fish, supplement with algae-derived DHA (at least 500 mg daily).

  3. Eat berries — especially blueberries — most days of the week. A half-cup to one-cup serving provides the anthocyanins and flavonoids that have been associated with delayed memory decline equivalent to 2.5 years in large prospective studies. Frozen berries retain their polyphenol content and are an economical option.

  4. Follow a MIND-diet-aligned pattern. Emphasize leafy greens (six or more servings per week), nuts (five servings per week), beans, whole grains, olive oil, and poultry. Limit red meat, butter, cheese, pastries, and fried foods. Even moderate adherence has been associated with meaningful cognitive protection.

  5. Ensure adequate B vitamin status. Eat leafy greens and legumes for folate, animal products or fortified foods for B12, and a varied diet for B6. If you are vegan, over 60, or have elevated homocysteine, consider a B-complex supplement.

  6. Incorporate curcumin regularly. Cook with turmeric plus black pepper and fat, or use a bioavailable curcumin supplement. Clinical trial evidence supports memory benefits at doses achievable with enhanced-absorption formulations.

  7. Minimize added sugar, ultra-processed foods, and excess alcohol. These are not merely unhelpful — they actively damage the hippocampus, suppress BDNF, and impair the biological machinery of memory at every stage from encoding to consolidation.

  8. Exercise aerobically at least 150 minutes per week. Exercise is the most powerful memory-enhancing intervention known, increasing hippocampal volume, BDNF, and neurogenesis. It amplifies every dietary strategy on this list.

  9. Protect your sleep. Seven to nine hours of quality sleep per night is non-negotiable for memory consolidation. Avoid caffeine after early afternoon, limit alcohol (which fragments sleep architecture), and maintain a consistent sleep schedule.

Frequently Asked Questions

Can specific foods actually improve memory, or just slow decline?

Both. In younger and middle-aged adults, the evidence suggests that optimizing nutrient intake (particularly choline, DHA, and flavonoids) supports better baseline memory performance — not just slower decline. In older adults, the evidence is predominantly about slowing decline and reducing dementia risk, though some interventions (such as DHA supplementation in the Yurko-Mauro 2010 trial) have demonstrated outright improvement in episodic memory. The practical distinction matters less than it might seem: whether you are building a better memory or preserving the one you have, the dietary strategies are the same.

How long does it take for dietary changes to affect memory?

Some effects are relatively rapid — DHA supplementation has shown memory improvements within 24 weeks in clinical trials, and blueberry juice studies have demonstrated benefits within 12 weeks. However, the most meaningful effects are cumulative and long-term. The Nurses’ Health Study data suggest that dietary patterns sustained over years produce the largest differences in cognitive trajectory. Think of a memory-supporting diet as a long-term investment in brain health rather than a quick fix.

Is the Mediterranean diet or the MIND diet better for memory?

The MIND diet was specifically designed for neuroprotection and, in observational studies, has shown stronger associations with cognitive outcomes than either the Mediterranean or DASH diets alone. Its particular emphasis on berries and leafy greens — the foods with the most consistent evidence for memory preservation — is what distinguishes it. That said, the Mediterranean diet is also strongly associated with cognitive protection, and any diet rich in fish, vegetables, fruits, nuts, olive oil, and whole grains while low in processed foods will capture the key memory-relevant nutrients.

Do memory supplements work?

Some have evidence. Citicoline and alpha-GPC provide bioavailable choline and have shown modest cognitive benefits in controlled trials. DHA supplements have demonstrated memory improvements in older adults with low baseline omega-3 status. Bioavailable curcumin formulations have shown benefits in an 18-month RCT. However, no supplement compensates for a poor overall diet, inadequate sleep, or physical inactivity. Supplements are best understood as potential additions to — not replacements for — the dietary and lifestyle foundation described in this article.

Does sugar actually damage memory, or just correlate with poor diet?

The evidence supports a direct, causal role. Animal studies demonstrate that high-sugar diets reduce hippocampal BDNF and impair memory within weeks, independent of other dietary factors. Human imaging studies show that higher blood glucose — even within the normal range — is associated with smaller hippocampal volume. The mechanisms (AGE formation, insulin resistance, BDNF suppression, neuroinflammation) are well-characterized and biologically plausible. While confounding is always a concern in observational human studies, the convergence of animal experimental evidence, human imaging data, and epidemiological findings makes a compelling case that excess sugar is directly harmful to memory systems.

Sources

  • Bowtell, J. L., Aboo-Bakkar, Z., Conway, M. E., Sherif, A., & Sherwood, R. A. (2017). Enhanced task-related brain activation and resting perfusion in healthy older adults after chronic blueberry supplementation. Applied Physiology, Nutrition, and Metabolism, 42(7), 773-779.
  • de Jager, C. A., Oulhaj, A., Jacoby, R., Refsum, H., & Smith, A. D. (2012). Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. International Journal of Geriatric Psychiatry, 27(6), 592-600.
  • Devore, E. E., Kang, J. H., Breteler, M. M. B., & Grodstein, F. (2012). Dietary intakes of berries and flavonoids in relation to cognitive decline. Annals of Neurology, 72(1), 135-143.
  • Erickson, K. I., Voss, M. W., Prakash, R. S., Basak, C., Szabo, A., Chaddock, L., … & Kramer, A. F. (2011). Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences, 108(7), 3017-3022.
  • Goncalves, N. G., Ferreira, N. V., Khandpur, N., Steele, E. M., Levy, R. B., Lotufo, P. A., … & Suemoto, C. K. (2023). Association between consumption of ultraprocessed foods and cognitive decline. JAMA Neurology, 80(2), 142-150.
  • Kerti, L., Witte, A. V., Winkler, A., Grittner, U., Rujescu, D., & Floel, A. (2013). Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology, 81(20), 1746-1752.
  • Krikorian, R., Shidler, M. D., Nash, T. A., Kalt, W., Vinqvist-Tymchuk, M. R., Shukitt-Hale, B., & Joseph, J. A. (2010). Blueberry supplementation improves memory in older adults. Journal of Agricultural and Food Chemistry, 58(7), 3996-4000.
  • Mander, B. A., Rao, V., Lu, B., Saletin, J. M., Lindquist, J. R., Ancoli-Israel, S., … & Walker, M. P. (2013). Prefrontal atrophy, disrupted NREM slow waves and impaired hippocampal-dependent memory in aging. Nature Neuroscience, 16(3), 357-364.
  • Molteni, R., Barnard, R. J., Ying, Z., Roberts, C. K., & Gomez-Pinilla, F. (2002). A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience, 112(4), 803-814.
  • Morris, M. C., Tangney, C. C., Wang, Y., Sacks, F. M., Barnes, L. L., Bennett, D. A., & Aggarwal, N. T. (2015). MIND diet associated with reduced incidence of Alzheimer’s disease. Alzheimer’s & Dementia, 11(9), 1007-1014.
  • Morris, M. C., Tangney, C. C., Wang, Y., Sacks, F. M., Bennett, D. A., & Aggarwal, N. T. (2015). MIND diet slows cognitive decline with aging. Alzheimer’s & Dementia, 11(9), 1015-1022.
  • Poly, C., Massaro, J. M., Seshadri, S., Wolf, P. A., Cho, E., Krall, E., … & Au, R. (2011). The relation of dietary choline to cognitive performance and white-matter hyperintensity in the Framingham Offspring Cohort. American Journal of Clinical Nutrition, 94(6), 1584-1591.
  • Small, G. W., Siddarth, P., Li, Z., Miller, K. J., Ercoli, L., Emerson, N. D., … & Barrio, J. R. (2018). 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. The American Journal of Geriatric Psychiatry, 26(3), 266-277.
  • Smith, A. D., Smith, S. M., de Jager, C. A., Whitbread, P., Johnston, C., Agacinski, G., … & Refsum, H. (2010). Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLOS ONE, 5(9), e12244.
  • Topiwala, A., Allan, C. L., Valkanova, V., Zsoldos, E., Filippini, N., Sexton, C., … & Ebmeier, K. P. (2017). Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study. BMJ, 357, j2353.
  • van Praag, H., Lucero, M. J., Yeo, G. W., Stecker, K., Heivand, N., Zhao, C., … & Bhargava, B. (2007). Plant-derived flavanol (-)epicatechin enhances angiogenesis and retention of spatial memory in mice. Journal of Neuroscience, 27(22), 5869-5878.
  • Walker, M. P., & Stickgold, R. (2006). Sleep, memory, and plasticity. Annual Review of Psychology, 57, 139-166.
  • Wu, A., Ying, Z., & Gomez-Pinilla, F. (2004). Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats. Journal of Neurotrauma, 21(10), 1457-1467.
  • Yurko-Mauro, K., McCarthy, D., Rom, D., Nelson, E. B., Ryan, A. S., Blackwell, A., … & Stedman, M. (2010). Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive decline. Alzheimer’s & Dementia, 6(6), 456-464.