Strong evidence exists to support the consumption of healthy, plant-based dietary patterns (e.g. Mediterranean, MIND or Nordic diet) for maintaining cognitive function and reducing dementia risk in later life and is supported by dementia prevention guideline from leading public health bodies (e.g. World Health Organization). Emerging evidence suggests potential cognitive benefits of consuming specific nutrients/foods (e.g. n-3 fatty acids or fish, flavonols and B-vitamins) and multi-nutrient compounds (e.g. Fortasyn Connect). Challenges and opportunities for integrating nutritional/dietary interventions for dementia prevention into clinical practice are explored in this review. 

The possibility of postponing or preventing dementia through nutritional and dietary habits has been increasingly investigated. In line with available epidemiological evidence, several nutritional compounds and regimens have shown to produce significant cognitive benefits among older persons enrolled in placebo-controlled studies. Nevertheless, despite these encouraging findings, robust supportive evidence is still lacking. In particular, further RCTs with long follow-up are needed in order to determine whether specific nutritional components or patterns may reduce the occurrence of cognitive disorders and overt dementing illnesses. In parallel, the clinical meaningfulness of the observed cognitive benefits, as measured by neuropsychological score changes, should be properly addressed and discussed. 

The ketogenic diet is low in carbohydrates and high in fat—a combination that increases the production of ketones, which have neuroprotective effects. Although it is a substantial overhaul of a typical diet, previous small studies suggest that following a ketogenic diet for a short duration can improve memory scores for people with mild cognitive impairment.61,62 One other pilot ketogenic diet trials that assesses brain outcomes is in progress now: a four-month trial of the Modified Mediterranean Ketogenic Diet (MMKD; NCT03472664) in 120 people with mild cognitive impairment. In 2019, a six-week trial of MMKD63 resulted in improvements of Alzheimer’s disease-related biomarkers and changes to the gut microbiome. There were no adverse effects, but the diet might be most feasible if prepared meals are provided to participants. 

One of the factors causing dementia is diet, namely macronutrient intake. Several studies have shown significantly that high carbohydrate and protein intake not only improves health but also improves cognitive function and memory in the elderly. Elderly people with excessive fat and saturated fatty acid intake are at higher risk of developing dementia. (1) Macronutrient intake (carbohydrates, fat, protein) is associated with dementia. (2) High carbohydrate intake can increase MMSE scores. (3) Excessive fat and saturated fat intake can increase the risk of dementia. (4) Sufficient protein intake can prevent abnormalities in amino acids that are useful for neurotransmitter synthesis.

A healthy diet can have a good effect on the brain, namely foods that contain protein, vitamins A, B6, B12, C, D, E, K. These foods include eggs, wheat, fruits, vegetables such as broccoli which are high in vitamin K, fish oil, seeds and nuts. A study published in the American Journal of Epidemiology showed that good vitamin E intake can help prevent cognitive decline, especially in the elderly.

This fifth research investigates the longitudinal relationships between omega-3 polyunsaturated fatty acid (PUFA) intake, blood biomarkers, and the risk of Alzheimer's disease (AD), dementia, or cognitive decline. It combines data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort with a meta-analysis of published cohort studies. 

Key Findings from the ADNI Cohort Study

• Supplementation and AD Risk: Long-term users of omega-3 fatty acid supplements showed a significant 64% reduced risk of AD (hazard ratio: 0.36, 95% confidence interval: 0.18, 0.72; P = 0.004). This protective effect was particularly noted in males, individuals of advanced age, those with the APOE ε4 genotype, and patients with mild cognitive impairment (MCI).

• Blood Markers: Plasma omega-3 fatty acids and their components were not significantly associated with AD risk in the ADNI cohort.

Key Findings from the Meta-Analysis

• Dietary Intake and Cognitive Decline: A moderate-to-high level of evidence suggests that dietary intake of omega-3 fatty acids can lower the risk of all-cause dementia or cognitive decline by approximately 20%.

  • DHA and EPA: Specifically, docosahexaenoic acid (DHA) intake was associated with an 18% lower risk (relative risk [RR]: 0.82, I² = 63.6%, P = 0.001). Each increment of 0.1 g/d of DHA or eicosapentaenoic acid (EPA) intake was associated with an 8%–9.9% (Plinear < 0.0005) lower risk of cognitive decline.

  • APOE ε4 Status: The protective effect of dietary omega-3 was observed in subgroups adjusted for APOE ε4 status.

• Blood Markers and Cognitive Decline: Moderate-to-high levels of evidence indicated that elevated levels of plasma EPA (RR: 0.88, I² = 38.1%) and erythrocyte membrane DHA (RR: 0.94, I² = 0.4%) were associated with a lower risk of cognitive decline.

  • Erythrocyte Membrane DHA: Higher levels of erythrocyte membrane DHA were significantly associated with a lower risk of cognitive decline (RR: 0.94, 95% CI: 0.89, 0.98; I² = 0.4%, Level H). 

Evidence Credibility: The evidence credibility for dietary intake and erythrocyte levels was higher than for plasma levels. Erythrocyte DHA is highlighted as a significant predictor of cognitive decline risk.