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Nutrients
Special Issues
The Role of Micronutrients in Neurodegenerative Disease
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The Role of Micronutrients in Neurodegenerative Disease

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

Deadline for manuscript submissions: 5 August 2024 | Viewed by 1041

Special Issue Editor

Prof. Dr. Panteleimon Giannakopoulos

E-Mail Website
Guest Editor
Department of Psychiatry, Faculty of Medicine, University of Geneva, 1205 Genève, Switzerland
Interests: Alzheimer’s disease; biomarkers; brain activation; magnetic resonance imaging; neurosciences; psychiatry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Degenerative diseases of the nervous system impose substantial medical and public health burdens on populations around the world. Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) are three major neurodegenerative diseases.

Nutrition plays an essential role in the pathogenesis and evolution of these diseases. Micronutrients, such as vitamins and minerals, are required in much smaller quantities than macronutrients, but are essential for numerous brain metabolic, biochemical, and regulatory processes. Both epidemiological and clinical evidence has shown that cognitive impairment and the risk of brain diseases associated with cognitive deficits can be lowered through the intake of specific micronutrients.  Several lines of evidence have showed that high levels of homocysteine and low levels of vitamin B12 and folate are associated with an increased risk of developing Alzheimer's disease. Moreover, markers of vitamin B12 status may predict very early CSF biomarker changes in this condition. From an etiological viewpoint, current research data support the idea that certain micronutrients are involved in key steps of the neurodegenerative process via the regulation of pathways invloved in oxidative stress (vitamins C and E), energy consumption, and inflammation (vitamin B in homocysteine metabolism),  but also  neuroendocrine, immunological, metabolic, and cardiovascular systems (flavonoids, polyunsaturated omega-3 fatty acids, and vitamin D)   that are critically implicated  in the prevention and treatment of neurodegenerative diseases.

This Special Issue provides a platform for researchers to discuss the role of micronutrients in neurodegenerative disease with the aim of helping to promote the development of this field. Papers, reviews, and/or clinical or experimental studies on the role of micronutrients in the preservation of cognitive function and the protection of the onset of neurodegenerative disease will be included.

Prof. Dr. Panteleimon Giannakopoulos
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

  • micronutrients
  • vitamins
  • minerals
  • dietary bioactive
  • neurodegenerative disease
  • Alzheimer's disease
  • Parkinson's disease
  • amyotrophic lateral sclerosis

Published Papers (1 paper)

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Research

17 pages, 3460 KiB  
Article
γ-Oryzanol from Rice Bran Antagonizes Glutamate-Induced Excitotoxicity in an In Vitro Model of Differentiated HT-22 Cells
by Li-Chai Chen, Mei-Chou Lai, Tang-Yao Hong and I-Min Liu
Nutrients 2024, 16(8), 1237; https://doi.org/10.3390/nu16081237 - 21 Apr 2024
Viewed by 668
Abstract
The excessive activation of glutamate in the brain is a factor in the development of vascular dementia. γ-Oryzanol is a natural compound that has been shown to enhance brain function, but more research is needed to determine its potential as a treatment for [...] Read more.
The excessive activation of glutamate in the brain is a factor in the development of vascular dementia. γ-Oryzanol is a natural compound that has been shown to enhance brain function, but more research is needed to determine its potential as a treatment for vascular dementia. This study investigated if γ-oryzanol can delay or improve glutamate neurotoxicity in an in vitro model of differentiated HT-22 cells and explored its neuroprotective mechanisms. The differentiated HT-22 cells were treated with 0.1 mmol/L glutamate for 24 h then given γ-oryzanol at appropriate concentrations or memantine (10 µmol/L) for another 24 h. Glutamate produced reactive oxygen species and depleted glutathione in the cells, which reduced their viability. Mitochondrial dysfunction was also observed, including the inhibition of mitochondrial respiratory chain complex I activity, the collapse of mitochondrial transmembrane potential, and the reduction of intracellular ATP levels in the HT-22 cells. Calcium influx triggered by glutamate subsequently activated type II calcium/calmodulin-dependent protein kinase (CaMKII) in the HT-22 cells. The activation of CaMKII-ASK1-JNK MAP kinase cascade, decreased Bcl-2/Bax ratio, and increased Apaf-1-dependent caspase-9 activation were also observed due to glutamate induction, which were associated with increased DNA fragmentation. These events were attenuated when the cells were treated with γ-oryzanol (0.4 mmol/L) or the N-methyl-D-aspartate receptor antagonist memantine. The results suggest that γ-oryzanol has potent neuroprotective properties against glutamate excitotoxicity in differentiated HT-22 cells. Therefore, γ-oryzanol could be a promising candidate for the development of therapies for glutamate excitotoxicity-associated neurodegenerative diseases, including vascular dementia. Full article
(This article belongs to the Special Issue The Role of Micronutrients in Neurodegenerative Disease)
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