Inhibition of Amyloid-Beta Production, Associated Neuroinflammation, and Histone Deacetylase 2-Mediated Epigenetic Modifications Prevent Neuropathology in Alzheimer's Disease
Alzheimer’s disease
amyloid-beta
cytokine release inhibitory drug 3
inflammation
mithramycin A
withaferin A
Journal
Frontiers in aging neuroscience
ISSN: 1663-4365
Titre abrégé: Front Aging Neurosci
Pays: Switzerland
ID NLM: 101525824
Informations de publication
Date de publication:
2019
2019
Historique:
received:
12
08
2019
accepted:
25
11
2019
entrez:
4
2
2020
pubmed:
6
2
2020
medline:
6
2
2020
Statut:
epublish
Résumé
Alzheimer's disease (AD) is a growing global threat to healthcare in the aging population. In the USA alone, it is estimated that one in nine persons over the age of 65 years is living with AD. The pathology is marked by the accumulation of amyloid-beta (Aβ) deposition in the brain, which is further enhanced by the neuroinflammatory process. Nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis. Histone deacetylase 2 (HDAC2)-mediated epigenetic mechanisms play a major role in the genesis and neuropathology of AD. Therefore, therapeutic drugs, which can target Aβ production, NLRP3 activation, and HDAC2 levels, may play a major role in reducing Aβ levels and the prevention of associated neuropathology of AD. In this study, we demonstrate that withaferin A (WA), an extract from
Identifiants
pubmed: 32009938
doi: 10.3389/fnagi.2019.00342
pmc: PMC6974446
doi:
Types de publication
Journal Article
Langues
eng
Pagination
342Informations de copyright
Copyright © 2020 Atluri, Tiwari, Rodriguez, Kaushik, Yndart, Kolishetti, Yatham and Nair.
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