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The Impact of Diet, Nutrition, and Lifestyle Habits on Cognition and the Risk of Developing Mild Cognitive Impairment and Dementia

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

Deadline for manuscript submissions: closed (25 July 2024) | Viewed by 863

Special Issue Editor


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Guest Editor
1. Fundación CITA-Alzheimer Fundazioa, 20009 Donostia, Spain
2. Osakidetza, Organización Sanitaria Integrada Debabarrena (OSI), 20690 Gipuzkoa, Spain
3. Department of Medicine, Faculty of Health Sciences, University of Deusto, 4800 Bilbo, Spain
Interests: neurodegenerative pathologies; Alzheimer's disease; sleep disorders; diet; lifestyle habits

Special Issue Information

Dear Colleagues,

More than a third of dementia cases could be preventable through the promotion of brain-healthy habits. Lifestyle habits include good adherence to a healthy diet, regular physical exercise, strict control of cardiovascular risk factors, promotion of good socioemotional health and engagement in continuous intellectual activity.

Advancing our understanding of the relationship between lifestyle habits and the risk of cognitive decline, as well as the progression from mild cognitive impairment to dementia, is crucial. It is imperative to understand the magnitude of risk increase or protection associated with each of these factors, and grasp their actual distribution within different populations (individuals at risk of cognitive decline, those with Alzheimer's disease and other causes of cognitive impairment, both in the general population and those with Down syndrome). Additionally, it is essential to comprehend the pathophysiological mechanisms through which these risk and protective factors operate, and assess their potential applicability as therapeutic targets for preventing cognitive decline (both degenerative and non-neurodegenerative) and managing the progression of cognitive impairment once established.

In this Special Issue, contributions focusing on healthy lifestyle habits are welcome, with a particular emphasis on those addressing diet and nutritional supplements in the context of a cognitive decline. Eligible submissions include works with a basic research approach (understanding the relationship between lifestyle habits and pathophysiological mechanisms related to the development of cognitive decline), translational research (the connection between these lifestyle habits, therapeutic strategies focused on promoting brain health and the relation with available biomarkers related with pathologies inducing cognitive decline) and clinical research (evaluating the effectiveness of interventions centered around lifestyle habits to prevent or mitigate cognitive decline). Original research, meta-analyses, systematic reviews and narrative reviews will all be considered.

Dr. Miren Altuna-Azkargorta
Guest Editor

Manuscript Submission Information

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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

  • lifestyle habits
  • diet
  • Alzheimer’s disease
  • cognitive decline
  • dementia
  • prevention

Published Papers (1 paper)

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Research

20 pages, 5931 KiB  
Article
Cholecalciferol Supplementation Impacts Behavior and Hippocampal Neuroglial Reorganization in Vitamin D-Deficient Rats
by Zsolt Gáll, Ágnes Csüdör, István-Gábor Sável, Krisztina Kelemen and Melinda Kolcsár
Nutrients 2024, 16(14), 2326; https://doi.org/10.3390/nu16142326 - 19 Jul 2024
Viewed by 640
Abstract
Vitamin D deficiency (VDD) is widespread around the world and has been extensively documented to affect various health conditions, including the cognitive functioning of the brain. Serum 25-hydroxylated forms of vitamin D are traditionally used to determine vitamin D status. However, there is [...] Read more.
Vitamin D deficiency (VDD) is widespread around the world and has been extensively documented to affect various health conditions, including the cognitive functioning of the brain. Serum 25-hydroxylated forms of vitamin D are traditionally used to determine vitamin D status. However, there is now evidence that cholecalciferol activation can occur and be controlled by locally expressed enzymes in the brain. This study aimed to investigate the effects of cholecalciferol supplementation on cognitive function in rats who underwent transient VDD in adulthood. Thirty-six adult Wistar rats were administered paricalcitol (seven doses of 32 ng injected every other day) along with a “vitamin D-free” diet to induce VDD, which was confirmed using a LC–MS/MS serum analysis of the cholecalciferol and 25-hydroxyvitamin D3 levels. Treatment was performed by including 1000 IU/kg and 10,000 IU/kg cholecalciferol in the diet. Cognitive performance was evaluated using the novel object recognition (NOR), Morris water maze (MWM), and radial arm maze (RAM) tests. An immunohistochemical analysis of the brain regions involved in learning and memory was performed by quantifying the neurons, astrocytes, and microglia labelled with anti-neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), and ionized calcium-binding adaptor molecule 1 (Iba-1) antibodies, respectively. The vitamin D deficient group showed the lowest performance in both the MWM and RAM tests. In contrast, the cholecalciferol-treated groups exhibited a faster learning curve. However, no difference was detected between the groups in the NOR test. On the other hand, differences in the cellular organization of the hippocampus and amygdala were observed between the groups. Cholecalciferol supplementation decreased the density of the Iba-1- and GFAP-labeled cells in the hilus and cornu Ammonis 3 (CA3) regions of the hippocampus and in the amygdala. These results support vitamin D’s substantial role in learning and memory. They also highlight that subtle changes of cognitive function induced by transient VDD could be reversed by cholecalciferol supplementation. Further studies are needed to better understand VDD and cholecalciferol’s effects on the brain structure and function. Full article
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