Neuroinflammatory Signaling in the Pathogenesis of Alzheimer's Disease.
Alzheimer’s disease
Neuroinflammation
astroglia
disease-associated microglia
inflammatory cytokine
microglia
Journal
Current neuropharmacology
ISSN: 1875-6190
Titre abrégé: Curr Neuropharmacol
Pays: United Arab Emirates
ID NLM: 101157239
Informations de publication
Date de publication:
2022
2022
Historique:
received:
06
12
2020
revised:
16
04
2021
accepted:
10
05
2021
pubmed:
17
9
2021
medline:
27
1
2022
entrez:
16
9
2021
Statut:
ppublish
Résumé
Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the formation of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment but also strongly interacts with immunological processes in the brain. On the other hand, aggregated and misfolded proteins can bind with pattern recognition receptors located on astroglia and microglia and can, in turn, induce an innate immune response, characterized by the release of inflammatory mediators, ultimately playing a role in both the severity and the progression of the disease. It has been reported by genome-wide analysis that several genes which elevate the risk for sporadic AD encode for factors controlling the inflammatory response and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of external factors which may interfere with the immunological mechanisms of the brain and can induce disease progression. In this review, we discussed the mechanisms and essential role of inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune processes and modulation of risk factors may lead to future therapeutic or preventive AD approaches.
Identifiants
pubmed: 34525932
pii: CN-EPUB-117499
doi: 10.2174/1570159X19666210826130210
pmc: PMC9199559
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
126-146Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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