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Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment
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Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: 5 April 2026 | Viewed by 9019

Special Issue Editor

Dr. Binosha Fernando

E-Mail Website
Guest Editor
Centre of Excellence for Alzheimer’s Disease Research & Care, School of Medical and Health Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, WA 6027, Australia
Interests: neurology; nutrition; microbiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the launch of a Special Issue focusing on the role of dietary supplements in neurodegenerative diseases, with an emphasis on nutritional assessment and their potential therapeutic impact. As neurodegenerative conditions such as Alzheimer’s disease, Parkinson’s disease, and other cognitive disorders continue to rise globally, there is an urgent need to explore how nutritional interventions and dietary supplements can influence disease progression, cognitive health, and patient outcomes.

This Special Issue welcomes original research articles, reviews, and clinical studies exploring:

  • The mechanistic roles of dietary supplements in neuroprotection.
  • Nutritional biomarkers and assessment tools in neurodegenerative diseases.
  • The impact of polyphenols, vitamins, omega-3 fatty acids, probiotics, and other bioactive compounds on cognitive decline.
  • Clinical and preclinical studies evaluating nutritional strategies for neurodegenerative disease management.
  • Gut–brain axis interactions and the influence of diet on neuroinflammation and brain ageing.

We invite researchers, clinicians, and nutrition scientists to contribute their work to this Special Issue and share cutting-edge insights into the role of dietary supplementation in brain health.

Submission Deadline: October 2025

For manuscript submission and further details, please visit our website.

We look forward to your valuable contributions!

Dr. Binosha Fernando
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegenerative conditions
  • nutritional biomarkers
  • gut–brain axis
  • probiotics
  • macro nutrients and micro nutrients

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Published Papers (4 papers)

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Research

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24 pages, 7132 KB  
Article
Early Oral Administration of D-Chiro-Inositol Reverses Hippocampal Insulin and Glutamate Signaling Deficits in the 3×Tg Humanized Mouse Model of Alzheimer’s Disease
by Beatriz Pacheco-Sánchez, Julia Verheul-Campos, Antonio Vargas, Rubén Tovar, Miguel Rodríguez-Pozo, Juan A. Navarro, Antonio J. López-Gambero, Elena Baixeras, Pedro J. Serrano-Castro, Juan Suárez, Carlos Sanjuan, Patricia Rivera and Fernando Rodríguez de Fonseca
Nutrients 2025, 17(18), 3024; https://doi.org/10.3390/nu17183024 - 22 Sep 2025
Viewed by 616
Abstract
Background and Objective: Humanized models of Alzheimer’s disease (AD) provide valuable tools for investigating the mechanisms of this neurodegenerative disorder, the leading cause of dementia. These models enable the study of AD progression and the potential disease-modifying properties of drugs or dietary nutrients [...] Read more.
Background and Objective: Humanized models of Alzheimer’s disease (AD) provide valuable tools for investigating the mechanisms of this neurodegenerative disorder, the leading cause of dementia. These models enable the study of AD progression and the potential disease-modifying properties of drugs or dietary nutrients delivered through nutrition. Here, we examine molecular markers of metabolic and synaptic dysfunction in the hippocampus of 6-month-old 3×Tg-AD mice and assess whether a dietary insulin sensitizer can delay synaptic decline. Methods: First we characterized the molecular phenotype of 3×Tg-AD at 12 months using shotgun proteomics and phosphoproteomics to assess metabolic and synaptic changes in the hippocampus. Then, we characterized the effects of early daily oral D-chiro-inositol (DCI, Gyneos®) for three months, starting at 3 months of age, to test restoration of insulin signaling and glutamatergic synaptic markers. To this end we evaluated a) insulin signaling pathway components (insulin receptor, IRS1, PI3K, AKT, GSK3β) at mRNA, protein, and phosphorylation levels, and b) the expression of glutamate receptors (mGluR5, GluR1, GluR2, NMDAR1, NMDAR2A, NMDAR2B). Sex effects were explored. Results: 12-month 3×Tg-AD mice exhibit metabolic and synaptic dysfunction in the hippocampus, with phosphoproteomic changes suggesting altered glutamatergic synapses. At 6 months, disruptions in insulin signaling were evident, including altered expression and phosphorylation of insulin pathway components, and changes in glutamate receptor subunits. Early DCI treatment largely reversed these alterations. Several effects showed sex dependency. Conclusions: Early insulin-sensitizing intervention via DCI can restore insulin signaling and counteract hippocampal synaptic impairments in this AD model, supporting the potential for nutrient-based strategies to delay synaptic decline. Sex differences underscore the need to tailor therapeutic approaches in modifying AD progression. Full article
(This article belongs to the Special Issue Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment)
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16 pages, 647 KB  
Article
Effects of Oral Anthocyanin Supplementation on In Vitro Neurogenesis, Hippocampus-Dependent Cognition, and Blood-Based Dementia Biomarkers: Results from a 24-Week Randomized Controlled Trial in Older Adults At Risk for Dementia (ACID)
by Chiara de Lucia, Diego Alejandro Tovar-Rios, Khadija Khalifa, Silje Meihack Kvernberg, Ilaria Pola, Anne Katrine Bergland, Jodi Maple-Grødem, Richard Siow, Nicholas Ashton, Clive Ballard, Sandrine Thuret and Dag Aarsland
Nutrients 2025, 17(16), 2680; https://doi.org/10.3390/nu17162680 - 19 Aug 2025
Viewed by 1246
Abstract
Background: Identifying compounds with neuroprotective properties that target the neurogenic process will have a considerable impact on dementia prevention. Methods: This is a secondary analysis of a 24-week randomised, double-blind, placebo-controlled anthocyanin supplementation trial in 181 participants. Using blood-derived serum collected during this [...] Read more.
Background: Identifying compounds with neuroprotective properties that target the neurogenic process will have a considerable impact on dementia prevention. Methods: This is a secondary analysis of a 24-week randomised, double-blind, placebo-controlled anthocyanin supplementation trial in 181 participants. Using blood-derived serum collected during this trial, we treated hippocampal progenitor cells and analysed the ensuing cellular changes in the context of the participant’s clinical and blood-based biomarker data. Results: We show that anthocyanin supplementation impacts hippocampal progenitor cells and that this can impact hippocampal-dependent cognition. We also show for the first time that blood-based dementia biomarkers correlate with human in vitro neurogenesis markers. Conclusions: Our data demonstrates moderator effects of BMI and ApoE4 carrier status and supports the need for more individualised trials. Further studies are warranted to explore the mechanism of action of anthocyanins and the use of blood-based biomarkers for clinical trial enrichment, trial individualization, and therapy development. Trial registration: NCT03419039; date first registered: 15/01/2018. Full article
(This article belongs to the Special Issue Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment)
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Review

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21 pages, 331 KB  
Review
Coenzyme Q10 and Cognition: A Review
by Madeleine C. Nankivell, Franklin Rosenfeldt, Andrew Pipingas, Matthew P. Pase, Jeffery M. Reddan and Con Stough
Nutrients 2025, 17(17), 2896; https://doi.org/10.3390/nu17172896 - 8 Sep 2025
Viewed by 4173
Abstract
Background and Objective: With an increase in the number of older citizens in most Western countries, cognitive decline is becoming an increasingly significant issue. Numerous age-related metabolic and physiological changes, such as increased inflammation and oxidative stress, decreased adenosine triphosphate (ATP) production, poorer [...] Read more.
Background and Objective: With an increase in the number of older citizens in most Western countries, cognitive decline is becoming an increasingly significant issue. Numerous age-related metabolic and physiological changes, such as increased inflammation and oxidative stress, decreased adenosine triphosphate (ATP) production, poorer cardiovascular function, and reduced cerebral blood flow, have been implicated in cognitive decline, prompting research into interventions. Among these, Coenzyme Q10 (CoQ10), an antioxidant and metabolic stimulant, has shown promise in improving some of the underlying biological mechanisms of cognitive decline. However, not much is known about the efficacy of CoQ10 supplementation on cognition in the elderly. Therefore, the aim of this review is to explore the efficacy of CoQ10 supplementation on cognitive function. Methods: We conducted a review of animal studies and human clinical trials investigating the effect of CoQ10 supplementation on cognition in samples who were healthy or with specific diseases. Overall, twelve studies demonstrated improved cognitive function and two showed a reduction in oxidative stress in response to CoQ10 supplementation, either alone or in combination with other compounds. Out of eight human clinical trials in healthy subjects (n = 2) and disease states (n = 6), four showed evidence of a beneficial effect of CoQ10 supplementation on cognition, while two demonstrated an increase in cerebral blood flow. Disparity in the results of the clinical trials presented here is likely due to differing testing procedures, inconsistent use of cognitive assessments, and/or varying bioavailability of different preparations of CoQ10. Conclusions: There is some evidence to suggest that cognition and the biological mechanisms that regulate it are positively impacted by CoQ10 therapy. However, it is crucial to note that the literature presents mixed results, with many human clinical trials also reporting no benefit of CoQ10 supplementation on cognitive performance. To fully evaluate the benefits of CoQ10 on cognitive function in ageing and in neurodegenerative diseases, future studies are needed that target possible mechanisms and utilise a wider range of cognitive assessments. Full article
(This article belongs to the Special Issue Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment)
30 pages, 932 KB  
Review
The Therapeutic Potential of Butyrate and Lauric Acid in Modulating Glial and Neuronal Activity in Alzheimer’s Disease
by Rathnayaka Mudiyanselage Uththara Sachinthanie Senarath, Lotta E. Oikari, Prashant Bharadwaj, Vijay Jayasena, Ralph N. Martins and Wanakulasuriya Mary Ann Dipika Binosha Fernando
Nutrients 2025, 17(14), 2286; https://doi.org/10.3390/nu17142286 - 10 Jul 2025
Viewed by 2329
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β plaque accumulation, tau tangles, and extensive neuroinflammation. Neuroinflammation, driven by glial cells like microglia and astrocytes, plays a critical role in AD progression. Initially, these cells provide protective functions, such as debris [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β plaque accumulation, tau tangles, and extensive neuroinflammation. Neuroinflammation, driven by glial cells like microglia and astrocytes, plays a critical role in AD progression. Initially, these cells provide protective functions, such as debris clearance and neurotrophic support. However, as AD progresses, chronic activation of these cells exacerbates inflammation, contributing to synaptic dysfunction, neuronal loss, and cognitive decline. Microglia release pro-inflammatory cytokines and reactive oxygen species (ROS), while astrocytes undergo reactive astrogliosis, further impairing neuronal health. This maladaptive response from glial cells significantly accelerates disease pathology. Current AD treatments primarily aim at symptomatic relief, with limited success in disease modification. While amyloid-targeting therapies like Aducanumab and Lecanemab show some promise, their efficacy remains limited. In this context, natural compounds have gained attention for their potential to modulate neuroinflammation and promote neuroprotection. Among these, butyrate and lauric acid are particularly notable. Butyrate, produced by a healthy gut microbiome, acts as a histone deacetylase (HDAC) inhibitor, reducing pro-inflammatory cytokines and supporting neuronal health. Lauric acid, on the other hand, enhances mitochondrial function, reduces oxidative stress, and modulates inflammatory pathways, thereby supporting glial and neuronal health. Both compounds have been shown to decrease amyloid-β deposition, reduce neuroinflammation, and promote neuroprotection in AD models. This review explores the mechanisms through which butyrate and lauric acid modulate glial and neuronal activity, highlighting their potential as therapeutic agents for mitigating neuroinflammation and slowing AD progression. Full article
(This article belongs to the Special Issue Dietary Supplement in Neurodegenerative Diseases: Nutritional Assessment)
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