Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression
Abstract
1. Introduction
2. Methods
3. Current Evidence
3.1. Dietary Patterns, ApoE4, the Gut Microbiome and Dementia Risk
3.1.1. Mediterranean, DASH and MIND Diet
3.1.2. Ketogenic Diet
3.2. ApoE4 and Nutrition
3.3. The Role of the Gut Microbiome and Malnutrition in Precision Nutrition
4. Nutrient–Gene Interactions as Potential Targets for Precision Nutrition and Dementia
4.1. Omega-3 Polyunsaturated Fatty Acids
4.2. Vitamin D
4.3. B6, B9 and B12 Vitamins
5. Considerations for Precision Nutrition in Dementia
5.1. Pharmacological Considerations: Malnutrition, Gut Microbiome and Polypharmacy
5.2. Direct-to-Consumer Genetic Testing
6. Advancing Precision Nutrition in Dementia: Opportunities and Solutions
6.1. Insights from Precision Nutrition Trials in Other Chronic Diseases to Inform Precision Nutrition in Dementia
6.2. The Role of Healthcare Professionals and Care Partners in Supporting Precision Nutrition
7. Artificial Intelligence in Dementia
7.1. Conceptual Applications of Artificial Intelligence in Precision Nutrition for Dementia
7.2. Wearable Sensor Technology and Biomarkers for Early Detection of Dementia
8. Future Directions and Limitations
8.1. Advances in Precision Nutrition for Dementia
8.2. Targeting Early Intervention, Genetic Diversity and Methodological Issues
8.3. Biomarker Discovery and Validation
8.4. Health Equity
9. Conclusions
Author Contributions
Funding
Conflicts of Interest
References
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Gut Microbiota Genera | AD Outcome | References |
---|---|---|
Collinsella | The APOE C rs429358 SNP genetic variant is positively correlated with Collinsella and AD diagnosis, independent of sex and age. | Cammann, et al. [36] |
Veillonella, Bacteroides and Lachnospira | Identified as a risk factor for AD. Bacteroides release pro-inflammatory liposaccharides capable of bypassing the mucosal barrier of the gastrointestinal tract endothelium leading to induced systemic inflammation. Liposaccharide-induced systemic inflammation is associated with synaptic loss and cognitive decline, with its role in AD pathophysiology well documented. | Cammann, et al. [36], Lukiw W.J [71], Zhan, et al. [72] |
Adlercreutzia, Eubacterium nodatum group, Eisenbergiella, Eubacterium fissicatena group, Gordonibacter, and Prevotella9 | Showed a negative correlation to AD diagnosis and were identified as having protective properties. | Cammann, et al. [36] |
Medication | Outcome | References |
---|---|---|
Donepezil (Cholinesterase Inhibitor) and Gastrointestinal Nutrient Absorption | A clinical trial with 188 people with mild-to-moderate AD, donepezil (5–10 mg daily) was associated with nausea, vomiting, and diarrhoea in 15–20% of participants, persisting after initial dose adjustment. | Rogers, et al. [103] |
Memantine and Vitamin D Metabolism | A randomised controlled trial investigated memantine (20 mg daily), an NMDA receptor antagonist, in 561 people with moderate-to-severe AD over 24 weeks. Memantine’s metabolism via cytochrome P450 enzymes in the liver was found to increase vitamin D metabolism, reducing its bioavailability. This led to lower serum 25-hydroxyvitamin D levels in 30% of treated participants compared to placebo, exacerbating bone health issues and potentially worsening cognitive outcomes. | Sano, et al. [104] |
Rivastigmine (Cholinesterase Inhibitor) and Protein Metabolism Interference | A 26-week open-label study of rivastigmine (3–12 mg daily) in 114 people with mild AD found that its cholinergic effects increased gastric acid secretion, altering protein digestion and amino acid absorption. The plasma levels of essential amino acids (e.g., tryptophan, tyrosine) dropped by 10–15% in 25% of participants, linked to nausea and appetite loss in 18% of cases. | Corey-Bloom J [105] |
Galantamine (Cholinesterase Inhibitor) and Iron Absorption Inhibition | A 26-week RCT of galantamine (8–24 mg daily) in 636 people with mild-to-moderate AD showed that its cholinergic stimulation of gastric motility reduced iron absorption by 15–20% in 35% of participants, as evidenced by lower ferritin levels. This was linked to nausea and altered gastric pH, affecting dietary iron bioavailability over time. | Raskind, et al. [106] |
Author | Perceived Barriers |
---|---|
Mathew et al., 2023 [131] | Nutrigenomic subjects should be a requirement in master’s level dietetic education |
Further research into precision nutrition is required for clinical implementation | |
Precision nutrition is a valuable tool for weight loss management | |
Genetic testing to inform precision nutrition strategies will improve medical nutrition therapy for diseases that require weight management | |
Nacis et al., 2022 [132] | Cost concerns |
Ethical considerations | |
It is a cellular approach to nutrition | |
Genes affect nutrient metabolism and nutrients affect genes | |
Greyvensteyn et al., 2022 [133] | Limited experts to convey professional advice |
Limited access to nutrigenomics for clients or patients | |
Do Rosario et al., 2025 [134] | Cost concerns (p < 0.001) |
Limited experts to convey professional advice (p < 0.001) | |
Limited ongoing education for healthcare professionals (p < 0.005) | |
Confidentiality concerns (p < 0.005) |
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Jewell, T.J.; Minehan, M.; Williams, J.; D’Cunha, N.M. Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression. J. Dement. Alzheimer's Dis. 2025, 2, 28. https://doi.org/10.3390/jdad2030028
Jewell TJ, Minehan M, Williams J, D’Cunha NM. Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression. Journal of Dementia and Alzheimer's Disease. 2025; 2(3):28. https://doi.org/10.3390/jdad2030028
Chicago/Turabian StyleJewell, Tara J., Michelle Minehan, Jackson Williams, and Nathan M. D’Cunha. 2025. "Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression" Journal of Dementia and Alzheimer's Disease 2, no. 3: 28. https://doi.org/10.3390/jdad2030028
APA StyleJewell, T. J., Minehan, M., Williams, J., & D’Cunha, N. M. (2025). Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression. Journal of Dementia and Alzheimer's Disease, 2(3), 28. https://doi.org/10.3390/jdad2030028