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Review

Precision Nutrition for Dementia: Exploring the Potential in Mitigating Dementia Progression

by
Tara J. Jewell
1,2,
Michelle Minehan
1,
Jackson Williams
1 and
Nathan M. D’Cunha
1,2,*
1
Discipline of Nutrition and Dietetics, University of Canberra, Bruce, ACT 2617, Australia
2
Centre for Ageing Research and Translation (CARAT), University of Canberra, Bruce, ACT 2617, Australia
*
Author to whom correspondence should be addressed.
J. Dement. Alzheimer's Dis. 2025, 2(3), 28; https://doi.org/10.3390/jdad2030028
Submission received: 9 April 2025 / Revised: 20 June 2025 / Accepted: 25 July 2025 / Published: 14 August 2025

Abstract

Precision nutrition is a tailored dietary approach that considers an individual’s genetic and metabolic profile, lifestyle factors, and specific nutritional needs to improve health and potentially modify disease progression. While research is ongoing into precision nutrition approaches for preventing dementia, there is no evidence on its targeted application to slow dementia-related disease progression and mitigate functional and cognitive decline. This narrative review addresses this gap by synthesising evidence on nutrient–gene interactions, genotype, gut microbiome, nutritional status and the interplay between metabolic pathways implicated in neuroinflammation and neurodegeneration to modify disease progression in a protective or therapeutic manner. Understanding and addressing comorbidities that share pathological mechanisms with dementia have the potential to enhance the understanding of precision nutrition to inform more effective, tailored approaches to slow dementia progression. To increase the robustness of precision nutrition trials for people with dementia, further research is needed into biomarker discovery, multi-omics technologies, and increasing mechanistic research to map the precise biological pathways underpinning the interactions between diet, gene expression, and neuroinflammation. Moreover, there is a need to evaluate the feasibility of precision nutrition for people experiencing cognitive impairment. Addressing these gaps will determine if people with dementia can benefit from precision nutrition and, subsequently, improve their quality of life and health outcomes.

1. Introduction

Dementia is an incurable neurological syndrome that describes a group of symptoms leading to progressive cognitive impairment [1]. Alzheimer’s disease (AD) is the most common form of dementia, though subtypes such as vascular dementia, Lewy body dementia, and frontotemporal dementia exist, each with distinct neuropathologies [2]. Dementia affects 55 million people worldwide, with 10 million new cases diagnosed each year [2]. The global population aged 60 and over is projected to double to 2.1 billion by 2050 [3], increasing the global prevalence of dementia. As a significant contributor of death, disability and dependency, the rising prevalence of dementia presents a major public health challenge [2].
Precision nutrition, or personalised nutrition, aims to offer individualised dietary strategies to prevent or mitigate disease progression by considering an individual’s unique genetic and metabolic profile [4]. On one hand, precision nutrition is guided by nutrigenomics, which targets neuropathological mechanisms of dementia that contribute to dementia onset and progression by understanding how nutrients influence gene expression, transcripts, and metabolic pathways [4,5]. On the other hand, nutrigenetics focuses on examining genetic variations (genotypic composition), particularly single-nucleotide polymorphisms (SNPs), and how these variations impact an individual’s response to dietary intake (phenotypic response) or nutritional interventions [6,7]. Both contribute to the bi-directional relationship between nutrient and gene interactions and form the basis of precision nutrition [7].
In addition to nutrigenomics and nutrigenetics, multi-omics technologies inform precision nutrition strategies by providing a system-level understanding of nutrient interactions within the body. Multi-omics technologies are defined as a thorough evaluation of select biological molecule types, combined with advanced computational techniques [8,9]. They include nutritional metabolomics (metabolite presence), transcriptomics (RNA expression), epigenomics (DNA methylation and histone modifications), proteomics (protein expression) and lipidomics (cellular functions) [5,6,10,11,12]. The integration of artificial intelligence (AI) with multi-omics technologies enables advanced computational techniques to further uncover complex patterns within multidimensional biological data [13].
The influence of precision nutrition on modifiable risk factors, defined as lifestyle and environmental influences that can reduce disease risk, is well established; however, its precise role in genetics and disease pathophysiology remains an area of ongoing exploration [14]. The most common causative genes of AD, Presenilin 1 (PSEN1), Presenilin 2 (PSEN2), and Amyloid Precursor Protein (APP), are characterised by the formation of intraneuronal neurofibrillary tangles due to tau hyperphosphorylation, misfolding and aggregation of amyloid peptides [5]. This results in progressive neuronal damage and the accumulation of extracellular amyloid-β (Aβ) plaques, a hallmark of AD [15]. Precision nutrition targets genetic risk factors to reduce dementia progression, or targets genetic expression observed in metabolic pathways related to dementia pathophysiology.
Research investigating a subset of 93 genes associated with dementia, metabolism and diet showed higher median expression levels in metabolically active tissues, particularly the thyroid, small intestine (terminal ileum), and adipose tissue (subcutaneous and visceral), compared to corresponding regions of the brain, such as the cerebellum, cervical spinal cord (C1), substantia nigra and cerebellar hemisphere [16]. For example, the Colony-stimulating Factor-1 Receptor (CSF1R) gene, identified for its role in microglial dysfunction and progressive dementia [17], was expressed in subcutaneous adipose tissue and cervical spinal cord (C1) with a blood–brain ratio of 0.877. The Ephrin Type-A Receptor 1 (EPHA1) gene, which may increase risk of AD, is expressed in the thyroid and cerebellum with a blood–brain ratio of 0.811 and involved in synaptic plasticity and immunity [18]. Genes with moderate blood–brain ratios (0.5–1.0) show increased expression in metabolically active peripheral tissues, potentially compensating for reduced brain expression. The redistribution of genetic expression suggests a regulatory mechanism influenced by diet, with peripheral metabolically active tissues modulating gene activity [16]. For instance, the APOE gene exhibits 1.9- to 2.8-fold higher expression in the liver than in the brain. Analysis of whole blood samples revealed correlations between 70 dietary factors and dementia-related gene expression, notably HMOX1 with manganese, bananas, quercetin, and tea, indicating the role of diet in brain health [16]. Bioactive food compounds, such as polyphenols and B vitamins, have been explored for their neuroprotective effects due to the role of nutrients as epigenetic regulators that alter the epigenome [19,20]. Identifying nutrition-specific factors offers opportunities for targeted gene–environment interventions to modulate dementia progression [21] by targeting underlying biological mechanisms involved in dementia pathophysiology [5,15].
Global shifts in food systems and lifestyles have contributed to the growing prevalence of ultra-processed foods (UPFs), defined as industrially manufactured, energy-dense food products with low nutritional value [22]. Evidence exploring UPFs and adverse health outcomes is increasing; for instance, a meta-analysis examining the impact of high UPF consumption reported an increased risk of all-cause dementia (95% CI: 1.09, 1.90; p = 0.02) [22]. The convenience of UPFs may serve as a convenient source of nutrition for people with dementia in stages where cognitive impairment influences functional and cognitive symptoms, contributing to reduced ability to prepare meals. This progressive decline in cognitive and physical function contributes to changed eating behaviours and increases the susceptibility to malnutrition [23,24,25]. Changed eating behaviours can result in inadequate dietary intake, increasing the risk of nutrient deficiencies, malnutrition, and dehydration, which is correlated with increased cognitive decline [23,24,26]. A meta-analysis investigating the global prevalence of malnutrition in people with dementia found that 47% of older people with dementia are at risk of malnutrition and a further 33% are malnourished, highlighting the prevalence of malnutrition and the potential for further cognitive decline in people with dementia [27]. There is an association between poor nutrition status and behavioural and psychological symptoms of dementia (BPSD) [28,29,30]. However, the strength of evidence varies as the studies are predominantly or wholly in women, lack detailed nutrient intake information and use a cross-sectional design, therefore limiting causal inference. Slowing dementia progression is important for the person affected by maintaining or improving their quality of life, independence [31], engagement in meaningful activities, and social connections [32]. The importance extends to societal factors such as reducing the economic costs associated with dementia care (direct and indirect healthcare costs) and alleviating care partner challenges [33].
Despite an increasing focus on precision nutrition, the biological mechanisms driving nutrient–gene interactions and their impact on dementia onset and progression remain unclear. Emerging evidence indicates that dietary factors may influence genetic expression and metabolic pathways relevant to dementia, but their potential for precision nutrition strategies to slow dementia-related disease progression and mitigate functional and cognitive decline is not well established. Therefore, this review aimed to (1) examine the biological basis of precision nutrition for slowing dementia progression, (2) evaluate the current evidence on precision nutrition and conditions that share pathological mechanisms with dementia, and (3) outline key considerations and future research directions for its application in dementia. Key themes include dietary patterns, ketogenic diets, Apolipoprotein E4 (ApoE4)-related dietary adjustments, gut microbiome interactions, and nutrient–gene interactions and has been summarised in Figure 1.

2. Methods

In January 2025, a non-systematic literature search was conducted using the Google Scholar, PubMed and Web of Science electronic databases. The search strategy included the terms “precision nutrition and dementia”, “personalised nutrition and dementia”, “nutrigenomics and dementia” and “multi-omics technologies and dementia”. The inclusion criteria included peer-reviewed journal articles and grey literature (e.g., nutrition guidelines) published in English focused on precision nutrition for dementia and common comorbidities that share pathological mechanisms with dementia. The reference lists of articles identified through the electronic database search were searched to identify additional relevant articles. Mechanistic, computational, or animal studies were omitted when examining the literature on nutrient–gene interactions. The findings were synthesised thematically, focusing on shared mechanisms and translatable insights to examine the potential of precision nutrition to slow dementia-related disease progression and mitigate functional and cognitive decline.

3. Current Evidence

Over the last decade, dietary patterns have come into focus for their potential to impact brain health; however, high-quality evidence supporting dietary interventions for people with dementia remains limited. Current guidelines established by the European Society for Clinical Nutrition and Metabolism outline forty recommendations on nutrition and hydration in dementia to prevent and treat malnutrition and dehydration, including care organisation requirements, professional healthcare training, and nutritional screening tools [34]. Recommendation 21 highlights the importance of individualised dietary counselling by a nutrition expert, acknowledging that no diet slows dementia progression, reinforcing the general recommendation to follow a healthy, balanced diet [34]. While the guidelines provide a framework for addressing malnutrition and dehydration in people with dementia, they do not incorporate genetic or multi-omics-based evidence. Recommendation 31 acknowledges the potential role of the ApoE4 genotype in modulating omega-3 (n-3) polyunsaturated fatty acid (PUFA) metabolism, but no dietary strategies are proposed. Given the growing body of evidence indicating that ApoE4 carriers may have altered lipid metabolism [35], the absence of guidance on personalised dietary modifications represents a gap in the guidelines and demonstrates the infancy of precision nutrition in dementia. Similarly, Recommendation 32 states probiotics should not be routinely offered to people with dementia to prevent or correct cognitive impairment, but does not sufficiently acknowledge the emerging role of gut microbiota in dementia pathophysiology or the role of AD-specific genetic variances such as ApoE4 in disrupting gut microbiota composition [36]. Future guidelines should consider incorporating emerging evidence for multi-omics technologies, such as lipidomics with ApoE4 genotype metabolism, to refine recommendations.
Dietary patterns such as the Mediterranean diet, the Dietary Approaches to Stop Hypertension (DASH) diet, and when combined, the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, are the most extensively researched for reducing cognitive decline [37]. Robust evidence on their neuroprotective effects in slowing dementia progression after diagnosis remains limited [25,34]. In addition to population-based dietary patterns, the neuroprotective potential of bioactive food compounds such as n-3 PUFAs, vitamin D, and B vitamins continues to be explored. However, the precise mechanisms through which they may influence dementia progression remain unclear. Plant-derived bioactive compounds, such as ubiquinol, curcumin, resveratrol and quercetin, have gained attention for their potential to modulate molecular mechanisms and nutrient–gene interactions underpinning neurodegenerative diseases as an alternative to synthetic compounds; however, most studies are in vitro, and human trials remain limited in scale and long-term follow-up, leading to inconclusive associations [38].

3.1. Dietary Patterns, ApoE4, the Gut Microbiome and Dementia Risk

3.1.1. Mediterranean, DASH and MIND Diet

The Mediterranean, DASH and MIND diets are plant-predominant dietary patterns that focus on consuming a variety of fruits, vegetables, grains, legumes, fish, low-fat dairy and limited lean meats, making it rich in fibre, PUFAs and polyphenols [37]. Adherence to healthy dietary patterns may reduce the rate of cognitive decline, and dementia or AD incidence [31,37,39,40]. Epidemiological studies evaluating the effectiveness of the Mediterranean, MIND or DASH diet often lack specific dietary intake data, are heterogeneous in design and are conducted in high-income countries, limiting their ability to determine causal relationships [31]. Several systematic reviews and human trials investigating the association between the Mediterranean or MIND diets and cognition or dementia report mixed results [41,42,43,44,45,46]. To date, most research has focused on dietary intake in relation to risk reduction and preventative strategies rather than treatment. Additionally, variability in dietary adherence and heterogeneity in study designs limit their applicability in assessing the impact of diet on dementia progression or the interpretation for precision nutrition strategies. It is possible that dietary patterns, such as the Mediterranean, DASH, or MIND diet, could mitigate dementia progression if adapted to follow a precision nutrition approach as this may also account for genetic variants that influence nutrient metabolism and brain health, such as ApoE4 status, which may enhance their efficacy for slowing dementia progression.
A three-year randomised controlled trial (RCT) found adherence to the MIND diet was positively associated with global cognitive function in older people with a family history of dementia but no cognitive impairment and that it may contribute to preserving cognitive function [47]. An RCT by Barnes et al. [43] assigned 604 participants without cognitive impairment with a family history of dementia to either a MIND-diet group or control-diet group from baseline to year 3 and found no significant estimated mean change in global cognition score in the MIND-diet group (95% CI: 0.164, 0.246) or control-diet group (95% CI: −0.130, 0.210) [43]. Similarly, Cornelis et al. [44] analysed data from the UK Biobank and found no significant associations between adherence to the MIND diet and improved cognitive health [44]. A systematic review and meta-analysis by Nucci et al. [41] reviewed 21 observational epidemiological studies (sample sizes: 96–28,025, age > 60), finding that adherence to the Mediterranean diet was associated with an 11% reduced risk of all-cause dementia (OR 0.89, 95% CI: 0.84, 0.94) and a 27% reduced risk of AD (OR 0.73, 95% CI: 0.62, 0.85) [41]. In addition to contrasting results, adherence to healthy dietary patterns can be challenging for people with dementia due to reduced cognitive function and altered eating behaviours [1,25,26].
As the role of genetic variants on nutrient metabolism becomes more established, incorporating precision nutrition approaches that adapt dietary patterns to a person’s unique genetic and metabolic background may offer an effective approach for dementia management.

3.1.2. Ketogenic Diet

Ketogenic diets restrict carbohydrate intake to <20–50 g/day [48] and are being explored for their therapeutic benefits in neurodegenerative conditions by shifting the brain’s primary fuel source from glucose to ketones [49]. A systematic review assessing the effects of ketogenic therapy on people with AD noted an improvement in long-term cognition, likely attributed to the ketones providing an altered energy source to neurons and their modulation of neuroinflammatory pathways such as oxidative stress [50]. A 2023 systematic review of seven studies in people aged 40+ years old on a ketogenic diet found statistically significant improvements in cognitive function in six of the studies, noting the only study not to reach statistical significance had low dietary adherence and a smaller sample size [51].
In addition to strict ketogenic diets, a modified Mediterranean–ketogenic diet has been explored for its potential role in modifying microbiome signatures associated with mild cognitive impairment (MCI), finding the diet to modulate gut microbiota and influence cognitive impairment [52]. Metabolomics and lipidomics can provide insight into individual responses to ketogenic diets by analysing ketone body utilisation, lipid metabolism and metabolic adaptations [53,54] in ApoE4 carriers, as the ApoE4 genotype may influence ketone body metabolism [50] and therefore has implications for precision nutrition strategies.

3.2. ApoE4 and Nutrition

ApoE4 is the strongest known genetic risk factor for developing AD [55,56] and is associated with neuropathological hallmarks, including tau tangles and Aβ plaque accumulation [1]. Individuals carrying one copy of the ApoE4 allele have a 3.7-times higher risk of developing AD, while those who are homozygous for ApoE4 have a 12-times higher risk [55]. The prevalence and genetic knowledge for ApoE4 carriers has led to an increase in seeking to ameliorate risk through lifestyle and nutrition interventions [49]. Precision nutrition specific to ApoE4 carriers has been considered due to the role of ApoE4 in dysregulating cholesterol gene expression and altered glucose metabolism [49,57].
Two human studies examined the effect of lipids according to ApoE genotype. The first study was a 16-week randomised, single-blinded dietary intervention with 120 participants who were ApoE4/E4 carriers with moderate cardiovascular risk and had lower total plasma cholesterol when replacing saturated fatty acids with monounsaturated, but not polyunsaturated fatty acids, with no changes in high-density lipoprotein-cholesterol or LDL-C [58]. The second study was the SATurated Fat and Gene APOE (SATgene) Study that recruited 100 participants with a BMI of 26 ± 3.8 and found ApoE3/E4 carriers had reduced plasma triglycerides with docosahexaenoic acid (DHA) supplementation, unlike ApoE3/E3 carriers [59]. Conversely, to investigate the relationship between AD risk, insulin resistance (IR) and dietary interventions, a randomised crossover pilot trial was conducted in participants with a mean age of 64, prediabetes and who were at risk of AD as determined by neuropsychologists and physicians [54]. The study had participants consume either a modified Mediterranean–ketogenic (5–10% carbohydrate < 20 g/day, 60–65% fat and 30% protein) or American Heart Association Diet (55–65% carbohydrate, 15–20% fat < 40 g/day and 20–30% protein) for six weeks. The six ApoE4 carriers in the study had no significant changes to their lipid profile after consuming a modified Mediterranean–ketogenic diet compared to non-ApoE4 carriers [54].
Insulin resistance is implicated in AD and type 2 diabetes mellitus (T2DM) [60]. Insulin is involved in key neuronal pathways, including glycogen synthase kinase-3β and phosphoinositide 3-kinase, which influence tau phosphorylation, Aβ production, and brain IR, critical aspects of AD pathology [61,62]. A large-scale genome-wide cross-trait analysis identified shared genetic loci between glycaemic traits and AD [63]. Compared to ApoE3, ApoE4 is associated with greater impairment of neuronal insulin signalling, contributing to AD-related metabolic dysfunction through mechanisms like lipid dysregulation and inflammation [35]. The term type 3 diabetes mellitus (T3DM) has been proposed to describe the overlapping cellular and molecular mechanisms of T2DM, IR, cognitive impairment, and AD [60]. This term is largely attributed to the mixed pathologies between AD and IR, positioning IR to be explored as a potential biomarker for AD [63]. A meta-analysis by Rashtchian et al. [64] encompassing 16 cohort, cross-sectional, and case–control studies with over 40,000 participants, found that ApoE4 carriers with T2DM have increased risk of dementia by 48% compared to non-diabetic ApoE4 carriers, and dementia frequency in ApoE4 carriers was 30% (95% CI: 0.15, 0.48).
The biological role of the ApoE4 genotype increases AD risk, and its impact on cholesterol metabolism and IR underscores the potential for precision nutrition interventions in ApoE4 carriers. Multi-omics technologies such as lipidomics, nutrigenomics and metabolomics may provide insight into these mechanisms by uncovering how ApoE4 influences lipid metabolism, IR and neuroinflammation at a molecular level, thereby informing targeted nutritional interventions that account for the many biological layers involved in metabolic dysfunction. Long-term trials of nutrition interventions in ApoE4 carriers are warranted to further inform precision nutrition for people with dementia.

3.3. The Role of the Gut Microbiome and Malnutrition in Precision Nutrition

Malnutrition, genetic variances and diet-induced dysbiosis are known to alter the gut microbiome [36,65,66,67]. Gut microbiota alterations can trigger pro-inflammatory factors capable of crossing the blood–brain barrier, promoting accumulation of Aβ plaques, and altered protein expression, strengthening the microbiota–gut–brain axis’s role in dementia pathophysiology [36,68,69]. The microbiota–gut–brain axis influences the gut microbiota state and brain through the enteric system and afferent signalling pathways, respectively [14]. Brain age, the functional and cognitive health of your brain compared to what is typical for your chronological age, also influences dysbiosis and cognitive performance, which has implications for age-related cognitive decline [70]. Table 1 describes specific gut microbiota genera and their associations to AD.
Dietary patterns rich in fibre, probiotics and prebiotics but limited in saturated fatty acids, processed foods and sugar, modulate the gut microbiota [73] and are associated with the development of dementia pathophysiology [69]. A systematic review of 17 observational and 20 interventional human studies in healthy subjects or those with metabolic disorders found higher microbial diversity amongst participants who adhered to a Mediterranean diet as opposed to a Western-type diet [74]. Insights into metagenomics, metabolomics, nutrigenomics, proteomics and transcriptomics may assist in discovering the complex interactions between genetic predisposition, dysbiosis and metabolic pathways influencing neuroinflammation to better understand the role of dysbiosis on dementia risk and progression. By targeting individual genetic, metabolic and microbial profiles of people with dementia, precision nutrition strategies may mitigate microbial disruptions, ultimately reducing neuroinflammation and modulating dementia progression.

4. Nutrient–Gene Interactions as Potential Targets for Precision Nutrition and Dementia

4.1. Omega-3 Polyunsaturated Fatty Acids

Bioactive omega-3 polyunsaturated fatty acids (n-3 PUFAs), DHA (C22:6) and eicosapentaenoic acid (EPA, C20:5) are often consumed through fatty fish, are present in neurons and glia, and have garnered attention due to their neuroprotective and anti-inflammatory properties. Both fatty acids maintain cellular membrane structure and functional integrity and are being explored for their role in neuroprotective pathways relevant to dementia, such as oxidative stress reduction [75,76,77,78].
Genetic variants of the Fatty Acid Desaturase (FADS) gene influence the rate-limiting pathways of PUFA biosynthesis [79]. FADS SNPs rs174557 and rs174547 are actively studied for their role in n-3 PUFA metabolism, with potential implications for cardiovascular disease [80], obesity and inflammation [81], which are comorbidities that may increase dementia risk [82,83]. A systematic review and meta-analysis found that A-allele carriers of the FADS1 SNP rs174556 were significantly negatively correlated with EPA and DHA blood concentrations, which are implicated in impaired cognitive function (95% CI: −0.189, 0.007, p = 0.036 and 95% CI: −0.174, −0.095, p < 0.001, respectively) [79]. Another mendelian randomisation study found that FADS1 and FADS2 gene expression in different brain regions (such as the cerebellum, cervical spinal cord (C1), hypothalamus and cortex) has a putative causal effect on cognitive function, suggesting FADS may be a potential target gene [84]. This is supported by a study that found that the T allele of the FADS1 SNP rs174556 significantly increased AD risk (95% CI: 1.23, 2.49, p = 0.001). Combined, polymorphisms of the FADS are particularly relevant for precision nutrition interventions [85].
The results from a systematic review of RCTs and observational studies suggest n-3 PUFA consumption before or during the early stages of cognitive decline could serve as a preventative strategy against AD [75]. Despite ongoing research into n-3 PUFAs on brain health, the efficacy of their role in dementia progression remains complex due to interindividual differences in nutrient metabolism and genetic predisposition. Healthy individuals with genotypic variances in ApoE4 were shown to influence the response to n-3 PUFA intake, with some evidence suggesting diminished benefits in ApoE4 carriers [86,87]. Additionally, differences in absorption, conversion efficiency from alpha-linolenic acid (ALA), and baseline dietary intake further complicate a one-size-fits-all approach.

4.2. Vitamin D

Vitamin D is investigated for its neuroprotective potential in improving cognitive function in people with MCI and dementia [88,89]. The Rush Memory and Aging Project, a community-based longitudinal study, suggests vitamin D deficiency (defined as circulating 25(OH)D3 < 10 ng/mL) and insufficiency (defined as circulating 25(OH)D3 10–19 ng/mL) are associated with a poorer global cognition (−0.007 standard units per year), and a proportionately higher risk of dementia and AD, particularly in people living in retirement communities as ApoE4 carriers without a dementia diagnosis [90]. Higher concentrations of 25(OH)D3 in the mid-frontal cortex, mid-temporal cortex, cerebellum and anterior watershed are associated with better working and semantic memory in participants who underwent postmortem brain analysis, with 40% diagnosed with dementia by the time of death [90].
One non-modifiable risk factor is a polymorphism of the Vitamin D Receptor (VDR) gene that converts vitamin D into its biologically active form (1,25-D3) [91]. VDRs are expressed in various brain regions, including the hippocampus and dentate gyrus, which are essential for memory and cognitive function [92]. A systematic review and meta-analysis by Liu et al. [93] investigated four SNPs of the VDR gene and found a potential association with MCI and AD [93]. People with polymorphisms Taql (rs731236) and Fokl (rs10735810) in the VDR gene may exhibit altered responses to vitamin D; therefore, tailoring vitamin D supplementation based on genetic predisposition could optimise therapeutic outcomes [94].
Accounting for vitamin D-based genetic variations in precision nutrition strategies for people with dementia may improve vitamin D status in people who are deficient [94]. This may be impactful for precision nutrition interventions due to the role 1,25-D3 has in the clearance of Aβ plaques, a hallmark of AD [92], and in modulating tau protein aggregation and hyperphosphorylation, a feature of young-onset frontotemporal dementia [95].

4.3. B6, B9 and B12 Vitamins

Elevated plasma total homocysteine, a nutrient-dependent and modifiable risk factor for dementia, is influenced by folate (B9), pyridoxine (B6) and cyanocobalamin (B12) status [96]. A systematic review of RCTs and observational intervention studies evaluated the efficacy of B complex vitamin supplementation in enhancing cognitive function in adults aged 45 or over [97]. Statistically significant benefits in cognitive function were observed in people with dementia when supplementing with B vitamins, especially folic acid [97]. These findings suggest that B vitamin supplementation may have benefits for people with vitamin B deficiency across different stages of dementia.
A retrospective case–control study evaluating postmortem brain tissue in 25 healthy people and 25 people with severe AD aimed to determine if genetics influenced folate metabolism and its association with AD [98]. The study found that the SNPs rs4633 and rs4680 of the Catelchol-O-methyltransferase (COMT) gene were strongly expressed in the postmortem brain tissue of people with AD compared to controls, and therefore may serve as predictors for AD (OR: 14.99, 95% CI: 2.024, 111.2 and OR: 12.00, 95% CI: 1.581, 91.084, respectively) [98]. The SNP rs1076991 in the methylene tetrahydrofolate dehydrogenase 1 (MTHFD1) gene was significantly associated as a risk factor for late-onset AD (OR: 14.00, 95% CI: 2.079, 94.24). MTHFD1 is involved in three crucial components of folate metabolism, suggesting SNPs have potential to alter folate metabolic pathways and subsequently increase homocysteine concentrations and risk of older-onset AD [98]. Similarly, polymorphism C677T in the Methylenetetrahydrofolate reductase (MTHFR) gene is associated with brain atrophy and elevated homocysteine levels, contributing to neurodegenerative mechanisms such as oxidative stress and inflammation [99]. Due to variability in nutrient–gene homocysteine metabolism, B vitamin supplementation should be a consideration for precision nutrition strategies for people with dementia.

5. Considerations for Precision Nutrition in Dementia

5.1. Pharmacological Considerations: Malnutrition, Gut Microbiome and Polypharmacy

Given the widespread use of dementia-related medications and the higher rates of polypharmacy among older adults, careful consideration must be given to pharmacology and precision nutrition [100]. Medications can influence nutrient absorption, metabolism and overall bioavailability, complicating the nutritional management of individuals with dementia and potentially impairing the therapeutic outcomes of prescribed treatments [101], summarised in Table 2. Malnutrition may alter drug metabolism, leading to either reduced efficacy [102] or increased toxicity of medications [101].
A systematic review and meta-analysis of RCTs, longitudinal studies and open-label trials found acetylcholinesterase inhibitors significantly contributed to weight loss between baseline and a median follow-up of 6 months (95% CI: p < 0.0001) in people with dementia [107]. Furthermore, polypharmacy has been shown to alter gut microbiome composition [108,109], which is increasingly investigated for its association with dementia progression and risk. Disruptions in gut microbial composition are associated with pathophysiological mechanisms of dementia, such as amyloid accumulation and neuroinflammation [110,111]. Recommendation 8 in The European Society for Clinical Nutrition and Metabolism guidelines advises replacing medications with adverse effects or reducing polypharmacy to mitigate potential causes of malnutrition in people with dementia [34]. Integrating precision nutrition in dementia requires consideration for the broader impact of nutrient–drug conflicts, including the broader impact of polypharmacy, malnutrition and drug-induced shifts in the gut microbiota.

5.2. Direct-to-Consumer Genetic Testing

The growing market for direct-to-consumer genetic testing (DTC-GT) has made genetic testing readily accessible to the public, operating independently of healthcare professionals [112]. Several DTC-GT companies market their products as tools to support genetically informed lifestyle modifications, such as precision nutrition and exercise plans [113] and vary in the type of genetic data they provide, the genetic testing technology they use and the cost of their service [114]. The incorporation of genetic testing to inform nutrition strategies is a maturing field, and the evidence base supporting genetically informed health insights is steadily developing. In one notable instance, concerns are raised about the limitations of DTC-GT services. For example, the quality of evidence substantiating some claims has been questioned, as companies may not sequence all possible genetic variants and could occasionally miss specific disease-linked variants, potentially leading to incomplete or misleading results [115,116]. However, elaborate genomic sequencing can be resource-intensive and may provide SNPs or genetic mutations without clinical significance. Isolated false-positive genetic testing results underscore the need for ongoing refinement in testing practices to establish the industry’s overall potential. Continued advancements in the DTC-GT sector may have implications for precision nutrition in future.

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

A multidisciplinary approach to precision nutrition may enable targeted nutritional strategies tailored to an individual’s genomic profile while simultaneously addressing other comorbidities commonly observed in people with dementia [85]. While several scoping and systematic reviews have explored the efficacy of precision nutrition, most focus on its applications for T2DM, metabolic syndrome, and obesity-related disorders with a focus on biomarkers such as blood glucose levels or lifestyle factors in lieu of genetic data [117,118,119,120]. The insights from these studies can be explored to see how precision nutrition may fit into a multidisciplinary care model for dementia and elicit behaviour change.
The perceived importance of nutrition among people with dementia and their care partners plays a crucial role in the uptake and success of targeted dietary interventions [121]. Low understanding of the benefits of nutrition can influence the efficacy of prescribed nutritional interventions, leading to low adherence [121]. While there is no direct evidence relating to people with dementia, a systematic review of controlled trials assessing the impact of precision nutrition on dietary intake in healthy adults aged between 18 to 79 found conveying genetic data does not significantly improve the effectiveness of precision nutrition strategies compared to approaches based on phenotypic and dietary analysis [122].
The Food4Me RCT reinforces this perspective, where they investigated behaviour changes amongst four groups with a mean age of 39.8 years through (1) general dietary advice per population guidelines, (2) personalised dietary advice per individual dietary intake, (3) personalised dietary advice per individual phenotypic data and (4) personalised dietary advice per individual phenotypic and genotypic data [123]. The study found no difference between the effectiveness of the precision nutrition intervention when including genotypic-based risk in communication to people, compared to standard dietary advice communication [123]. The Food4Me trial suggests that if dietary interventions are prescribed without explicitly detailing the underlying genomic analysis, adherence to the recommendations is unlikely to be affected [123]. This approach aligns with patient preference in medical information communication, where technical jargon or descriptive themes are not preferred or standard practice in healthcare [124]
Conversely, the Nutrigenomics, Overweight/Obesity and Weight Management (NOW) RCT evaluated the efficacy of providing genomic-based dietary advice for overweight individuals (BMI of ≥25 kg/m2) from the Group Lifestyle Balance (GLB) program [125]. The participants were randomly assigned to a standard GLB program (following Canada Health 2010 population-based dietary guidelines) or a modified GLB and nutrigenomic (GLB+NGx) program tailored to their nutrigenomic profiles. Screened genes included SNP rs1800592 of Mitochondrial uncoupling protein 1 (UCP1) to provide data on energy metabolism, SNPs rs9939609 and rs9939609 of Fat mass and obesity-associated (FTO) for protein, PUFAs and SFAs, rs7903146 of Transcription factor 7-like 2 (TCF7L2) for total fat, rs5082 of Apolipoprotein A2 (APOA2) for SFAs and rs17782313 of Melanocortin 4 receptor (MC4R) for snacking and appetite. The GLB+NGx group received genetic reports and were advised to adhere to one primary nutritional intervention. The primary outcome, body fat percentage change via bioelectrical impedance analysis, showed greater reductions in the GLB+NG group at 3 months (GLB+NGx: BFP −4.9% (95% CI −3.3, −6.6) compared to GLB: BFP −2.2% (95% CI: −0.5, −3.9)) and 6 months (GLB+NGx: −7.7% (95% CI: −5.8, −9.6) compared to GLB: BFP −4.8% (95% CI: −2.8, −6.8)) with participants maintaining recommended dietary fat consumption levels [125]. These findings suggest that genetically informed dietary advice effectively influences behaviour change. This was observed to a lesser degree in an RCT of 188 participants who were provided with their ApoE4 carrier status, resulting in minor beneficial lifestyle changes to improve health irrespective of ApoE4 status [126]. Despite genetic results leading to differences in behaviour change amongst participants, both the Food4Me trial and the NOW trial favoured health outcomes.
These contrasting findings highlight the complexity of using genetically informed dietary advice to influence behaviour change and underscore the importance of communication style and individual characteristics and preferences. In the case of dementia, where cognitive impairment may influence dietary adherence, it remains unclear whether receiving precision genetic information enhances or hinders dietary behaviour change. This gap presents an opportunity for future research to evaluate whether the inclusion or omission of genomic risk information in nutritional counselling affects dietary adherence and health outcomes in people with dementia. This will refine and adapt precision nutrition strategies to meet the practical needs of this population, ultimately improving care outcomes and supporting the future development of evidence-based guidelines for practice and policy if deemed an appropriate dietary strategy.

6.2. The Role of Healthcare Professionals and Care Partners in Supporting Precision Nutrition

The use of precision nutrition in dementia care models requires collaboration between healthcare professionals and people with dementia, including care partners and families. A thorough understanding and interpretation of genetic data will be essential for healthcare professionals to develop targeted nutrition strategies, ideally within a multidisciplinary team. Many clinicians, including dietitians, lack formal training in genomics, leading to challenges in interpreting and applying genetic results in clinical practice [127,128,129]. Addressing the educational gap of genetic testing literacy amongst clinicians is important to ensure accurate, evidence-based recommendations in precision nutrition for dementia while accounting for broader precision medicine applications [128,130]. Several studies have examined the perspectives of dietitians in integrating human genomics into clinical practice, viewable in Table 3 [131,132,133,134]. Across these studies, a clear consensus emerges; dietitians recognise the potential benefits and value of nutrigenomics in clinical settings, though often lack the necessary genetic background knowledge to apply it effectively. This is likely attributed to the limited utility of precision nutrition in clinical practice.
A qualitative study examining Australian genetic counsellors’ perspectives on their role in facilitating behaviour change following genetic testing revealed that while they provide genetic counselling, guiding clients through behavioural modifications falls beyond their scope of practice, governed by the Human Genetics Society of Australasia [135]. The findings highlight the need for a clearer distinction of responsibilities in healthcare, ensuring appropriate support for individuals navigating genetic insights and lifestyle adjustments [135].
To support multidisciplinary integration, educational resources such as nutrigenomics training modules and workshops can equip dietitians with the skills to interpret genetic reports and translate them into precision nutrition interventions, helping bridge the gap between precision nutrition and its practical application in healthcare. Similarly, explanatory printed materials and online platforms that simplify the principles of nutrigenomics can serve as essential tools for care partners who may lack an understanding of the significance of precision nutrition. A 2024 study analysed survey results from 46 participants in both a younger cohort (aged 25–44 years) and longitudinal cohort (aged 45–80 years) to determine their behaviour towards biomarker disclosure [136]. A clinician presented cognitive biomarker results (cerebrospinal fluid biomarkers, ApoE, tau and amyloid) via a telehealth appointment in conjunction with an educational presentation to detail biomarker status and subsequent clinical diagnosis and significance. Receiving results with an education resource was well received. Approximately 96% of participants were pleased to receive their biomarker status, and 85% of participants experienced low anxiety levels post results [136].
For precision nutrition to become more widely used, healthcare professionals need training in genetic literacy to accurately interpret data and provide advice. Educational resources for care partners, effective communication of biomarkers, and respect for genetic insight preferences are essential for supporting informed decision-making and tailored interventions for people with dementia.

7. Artificial Intelligence in Dementia

7.1. Conceptual Applications of Artificial Intelligence in Precision Nutrition for Dementia

As precision nutrition continues to evolve, the integration of AI, multi-omics technologies, and biomarker discovery will be instrumental in refining its application. The use of machine learning to identify meaningful patterns in the pathophysiology of dementia contextualises system biology, an interdisciplinary field that analyses several biological layers, such as genetic data and multi-omics technologies, to understand the dynamic interaction of a biological system rather than focusing on biological layers in isolation [13,137,138]. With system biology information, high-throughput data analysis and network-based approaches, AI may be used to identify biological patterns and reveal complex, connected mechanisms within the body that influence dementia progression [139]. Integrating and interpreting the biological layers of multi-omics technologies is highly intricate, making human mapping challenging. However, AI’s capacity to process vast quantities of data can reveal complex interactions between genes, metabolites, and environmental factors [140] that traditional research methods may overlook, potentially uncovering novel precision nutrition interventions to mitigate dementia risk and progression [13,140].
Convolutional Neural Networks have shown efficacy in processing neuroimaging data to detect early structural brain changes associated with dementia [141], while Support Vector Machines and Random Forest algorithms are applied to genetic and metabolic data to identify biomarkers associated with dementia-related diseases [142,143]. In the context of precision nutrition for people with dementia, AI can integrate diverse datasets to tailor dietary interventions based on genetic, metabolic and microbiome profiles. Furthermore, Natural Language Processing can explore clinical notes and client history to improve early detection and intervention strategies for cognitive impairment [144]. AI-driven precision interventions account for biological layers of data and may therefore be used as a tool to refine dietary recommendations to mitigate dementia progression based on an individual’s profile.

7.2. Wearable Sensor Technology and Biomarkers for Early Detection of Dementia

Wearable sensor technology for detecting nutrient-related biomarkers is a new development with implications for health management, particularly when integrated with multi-omics approaches in dementia care and precision nutrition. These devices continuously measure biochemical markers, including but not limited to glucose, vitamins, ketone bodies or amino acids, while multi-omics technologies provide a comprehensive view of an individual’s molecular profile. Utilising this information with high-throughput AI models may enhance and optimise the interpretation of nutritional data in people with dementia. This is important for dementia, where nutrient deficiencies like vitamin B12 or omega-3 fatty acids may accelerate cognitive decline. Combining wearable sensor data with multi-omics could detect imbalances early and inform targeted tailored dietary interventions to slow disease progression, allowing for longer durations of precision nutrition interventions.

8. Future Directions and Limitations

8.1. Advances in Precision Nutrition for Dementia

Precision nutrition in dementia is a field with significant potential due to current advancements in AI-powered precision medicine and genomic analysis. Research highlights the promise of tailoring dietary interventions to individual genetic profiles for dementia progression [140]. However, further development in AI technologies and digital health applications is essential to integrate precision nutrition into current healthcare practices [8,145,146,147]. The expansion of clinically validated SNP databases is required to increase the effectiveness of precision nutrition for dementia. Clinical evidence remains limited, highlighting the need for trials to evaluate feasibility and efficacy against conventional diets, with considerations for dietary adherence in people who experience cognitive impairment. Research has demonstrated the value of multidomain lifestyle interventions for cognitive improvement, yet nutrition’s specific effects are rarely isolated [148]. Bridging this gap is critical, as early dietary interventions targeting modifiable risk factors could slow dementia progression, given its decades-long neuropathological development [149].

8.2. Targeting Early Intervention, Genetic Diversity and Methodological Issues

Given the long prodromal phase of neurodegenerative diseases, future research should explore the potential of precision nutrition interventions in people under 65 years to better capture their long-term impact on dementia progression. Genetic predispositions other than ApoE4 warrant further investigation in dementia research, such as autosomal dominant mutations in chromosome 9 open reading frame (C9orf72), microtubule-associated protein tau (MAPT), and progranulin (GRN), which are implicated in frontotemporal dementia [150]. This recommendation is threefold: first, to broaden research efforts beyond older-onset AD and capture the heterogeneity of dementia subtypes; second, to explore the potential benefits of early targeted nutritional interventions in populations particularly vulnerable to early-onset neurodegeneration; and third, the implications of young-onset dementia subtypes are equally economically and socially burdensome as those of older-onset AD [151].
A 2024 scoping review highlighted significant gaps in care models for dementia, noting that they predominantly focus on people aged 65 and older while overlooking the unique needs of those with young-onset dementia, typically between the ages of 30 and 65 [152]. Since frontotemporal dementia often manifests at a younger age, there may be a greater window of opportunity for dietary strategies to improve long-term cognitive outcomes and disease trajectory. Expanding research to other forms of dementia is essential to broaden the application of nutritional strategies in people with dementia.
Large-scale trials of nutrition and dietary supplement interventions often have inconclusive or conflicting results due to the complexity of studying nutrition’s impact on cognition [89,153,154,155]. Complex factors include inaccurate food intake assessments, diverse dietary pattern scoring systems, lack of standardisation in cognitive decline measurement tools, useful biomarkers and insufficient follow-up periods to detect meaningful changes [156]. Traditional self-reported dietary data, such as 24 hour food recalls, food frequency questionnaires and food diaries, rely on an individual’s ability to recall food intake over a period of time, which may be problematic for people with dementia [157]. Dietary recall methods are prone to inaccuracies due to recall bias, social desirability bias, and underreporting [157]. For people with dementia, cognitive impairment, altered dietary habits, and complex nutritional needs further exacerbate these limitations, making self-reported data particularly unreliable [26]. In addition, to advance research into precision nutrition, barriers should be reduced to access large de-identified datasets from medical centres and institutions. This will require compliance with privacy regulations, secure data-sharing agreements, and simplified approval processes to empower researchers to accelerate advancements in precision nutrition.

8.3. Biomarker Discovery and Validation

Effective precision nutrition requires stronger evidence identifying blood-based or neuroimaging biomarkers to detect early dementia-related changes and optimise precision medicine interventions [158]. Existing biomarkers, such as CSF, tau and Aβ plaques, as well as neuroimaging markers, provide critical insights into disease pathology, but further research is needed to identify molecular and digital biomarkers linked to diet and dementia progression [159]. Advancements in multi-omics technologies may assist in the discovery of novel biomarkers that reflect dietary influences on neurodegeneration. Additionally, gut-microbiome-derived metabolites have emerged as potential biomarkers given their role in systemic inflammation and cognitive function [36,160]. Future research should prioritise integrating biomarker discovery with AI-driven analysis to identify patterns that predict dementia progression to inform precision nutrition strategies. By incorporating biomarker identification into trials with precision dietary interventions, researchers can better evaluate the efficacy of and their role in mitigating neurodegeneration and improving cognitive function.

8.4. Health Equity

Precision nutrition may offer tailored interventions for people with dementia [4] but these are often accessible only to those who have the financial, educational and systemic advantages necessary to engage [161]. Many risk factors for dementia, including air pollution exposure, traumatic brain injury, mental health status, education, social isolation, physical inactivity and hearing loss [31], are influenced by broader societal determinants of health and are beyond individual control. When precision nutrition is not feasible, population-based dietary guidelines remain effective for promoting overall health [37], though these often assume a certain level of nutritional literacy and food access that is not attainable for socioeconomically disadvantaged groups. Nutrition strategies, whether personalised or population-based, must consider societal and structural barriers to access to ensure inclusivity and equity. The future directions and limitations of precision nutrition for dementia has been summarised in Figure 2.

9. Conclusions

Precision nutrition in dementia care leverages genetics, metabolism, and environmental factors to support brain health, offering a targeted alternative to conventional dietary advice. Deepening the understanding of how diet modulates genetic and metabolic pathways implicated in neuroinflammation and dementia pathophysiology is necessary to accelerate the progress and uptake of precision nutrition for dementia. Clinical trials are needed to assess the feasibility and efficacy of precision nutrition interventions in slowing disease progression. Advancements in biomarker discovery, multi-omics technologies, nutrient–gene interactions and AI are critical for developing precision dietary interventions. Without these, robust evidence for the role of precision nutrition in mitigating dementia progression remains limited. Importantly, while precision nutrition for people with dementia may provide benefits, the long-term impact of dietary patterns, lifestyle factors and environmental exposure must also be addressed through targeted research.

Author Contributions

Conceptualisation, Methodology, and Investigation, T.J.J. and N.M.D.; Writing—Original Draft T.J.J.; Writing—Review and Editing N.M.D., M.M., and J.W.; Supervision N.M.D. and M.M. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

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Figure 1. The components of precision nutrition: precision nutrition integrates multiple biological, dietary, and environmental factors to tailor nutritional recommendations to individual needs. This figure highlights key omics technologies, including nutrigenomics, metabolomics, transcriptomics, epigenomics, proteomics, and lipidomics, alongside the gut microbiome and dietary patterns, which collectively influence nutrient metabolism, gene expression, and overall health outcomes. Created in BioRender. Jewell, T. (2025) https://BioRender.com/m2q15q7.
Figure 1. The components of precision nutrition: precision nutrition integrates multiple biological, dietary, and environmental factors to tailor nutritional recommendations to individual needs. This figure highlights key omics technologies, including nutrigenomics, metabolomics, transcriptomics, epigenomics, proteomics, and lipidomics, alongside the gut microbiome and dietary patterns, which collectively influence nutrient metabolism, gene expression, and overall health outcomes. Created in BioRender. Jewell, T. (2025) https://BioRender.com/m2q15q7.
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Figure 2. The future directions and limitations of pprecision nutrition for dementia: key domains influencing the advancement of precision nutrition for dementia: artificial intelligence, early intervention, genetic diversity, methodological considerations, biomarker discovery, and health equity.
Figure 2. The future directions and limitations of pprecision nutrition for dementia: key domains influencing the advancement of precision nutrition for dementia: artificial intelligence, early intervention, genetic diversity, methodological considerations, biomarker discovery, and health equity.
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Table 1. Gut microbiota genera and AD risk.
Table 1. Gut microbiota genera and AD risk.
Gut Microbiota GeneraAD OutcomeReferences
CollinsellaThe 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 LachnospiraIdentified 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 Prevotella9Showed a negative correlation to AD diagnosis and were identified as having protective properties.Cammann, et al. [36]
Table 2. Pharmacology and adverse outcomes in people with AD.
Table 2. Pharmacology and adverse outcomes in people with AD.
MedicationOutcomeReferences
Donepezil (Cholinesterase Inhibitor) and Gastrointestinal Nutrient AbsorptionA 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 MetabolismA 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 InterferenceA 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 InhibitionA 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]
Table 3. Key perceived concerns of precision nutrition amongst dietitians.
Table 3. Key perceived concerns of precision nutrition amongst dietitians.
AuthorPerceived 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

AMA Style

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 Style

Jewell, 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 Style

Jewell, 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

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