Gene Signals and SNPs Associated with Parkinson's Disease: A Nutrigenomics and Computational Prospective Insights.
Parkinson’s disease (PD)
SNP’s
neurodegenerative disease
nutrigenomics
Journal
Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074
Informations de publication
Date de publication:
21 11 2023
21 11 2023
Historique:
received:
02
03
2023
revised:
05
05
2023
accepted:
11
10
2023
medline:
13
11
2023
pubmed:
20
10
2023
entrez:
20
10
2023
Statut:
ppublish
Résumé
Parkinson's disease is the most prevalent chronic neurodegenerative disease. Neurological conditions for PD were influenced by a variety of epigenetic factors and SNPs in some of the coexisting genes that were expressed. This article focused on nutrigenomics of PD and the prospective highlighting of how these genes are regulated in terms of nutritive factors and the genetic basis of PD risk, onset, and progression. Multigenetic associations of the following genetic alterations in the genes of SNCA, LRRK2, UCHL1, PARK2,PINK1, DJ-1, and ATP13A2 have been reported with the familial and de novo genetic origins of PD. Over the past two decades, significant attempts have been made to understand the biological mechanisms that are potential causes for this disease, as well as to identify therapeutic substances for the prevention and management of PD. Nutrigenomics has sparked considerable interest due to its nutritional, safe, and therapeutic effects on a variety of chronic diseases. In this study, we summarise some of the nutritive supplements that have an impact on PD.
Identifiants
pubmed: 37858629
pii: S0306-4522(23)00457-8
doi: 10.1016/j.neuroscience.2023.10.007
pii:
doi:
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
77-95Informations de copyright
Copyright © 2023 IBRO. Published by Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.