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The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death

Alzheimer’s disease (AD) is accompanied by neural cell loss and memory deficit. Neural cell death, occurring via apoptosis and autophagy, is widely observed in the AD brain in addition to neuroinflammation mediated by necroptosis and the NLRP3 inflammasome. Neurotoxicity induced by amyloid-beta (Aβ)...

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Autores principales: Choi, Su-Bin, Kwon, Sehee, Kim, Ji-Hye, Ahn, Na-Hyun, Lee, Joo-Hee, Yang, Seung-Hoon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10380735/
https://www.ncbi.nlm.nih.gov/pubmed/37511515
http://dx.doi.org/10.3390/ijms241411757
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author Choi, Su-Bin
Kwon, Sehee
Kim, Ji-Hye
Ahn, Na-Hyun
Lee, Joo-Hee
Yang, Seung-Hoon
author_facet Choi, Su-Bin
Kwon, Sehee
Kim, Ji-Hye
Ahn, Na-Hyun
Lee, Joo-Hee
Yang, Seung-Hoon
author_sort Choi, Su-Bin
collection PubMed
description Alzheimer’s disease (AD) is accompanied by neural cell loss and memory deficit. Neural cell death, occurring via apoptosis and autophagy, is widely observed in the AD brain in addition to neuroinflammation mediated by necroptosis and the NLRP3 inflammasome. Neurotoxicity induced by amyloid-beta (Aβ) and tau aggregates leads to excessive neural cell death and neuroinflammation in the AD brain. During AD progression, uncontrolled neural cell death results in the dysregulation of cellular activity and synaptic function. Apoptosis mediated by pro-apoptotic caspases, autophagy regulated by autophagy-related proteins, and necroptosis controlled by the RIPK/MLKL axis are representative of neural cell death occurred during AD. Necroptosis causes the release of cellular components, contributing to the pro-inflammatory environment in the AD brain. Inordinately high levels of neural cell death and pro-inflammatory events lead to the production of pro-inflammatory cytokines and feed-forward hyper neuroinflammation. Thus, neural cell death and neuroinflammation cause synaptic dysfunction and memory deficits in the AD brain. In this review, we briefly introduce the mechanisms of neural cell death and neuroinflammation observed in the AD brain. Combined with a typical strategy for targeting Aβ and tau, regulation of neural cell death and neuroinflammation may be effective for the amelioration of AD pathologies.
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spelling pubmed-103807352023-07-29 The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death Choi, Su-Bin Kwon, Sehee Kim, Ji-Hye Ahn, Na-Hyun Lee, Joo-Hee Yang, Seung-Hoon Int J Mol Sci Review Alzheimer’s disease (AD) is accompanied by neural cell loss and memory deficit. Neural cell death, occurring via apoptosis and autophagy, is widely observed in the AD brain in addition to neuroinflammation mediated by necroptosis and the NLRP3 inflammasome. Neurotoxicity induced by amyloid-beta (Aβ) and tau aggregates leads to excessive neural cell death and neuroinflammation in the AD brain. During AD progression, uncontrolled neural cell death results in the dysregulation of cellular activity and synaptic function. Apoptosis mediated by pro-apoptotic caspases, autophagy regulated by autophagy-related proteins, and necroptosis controlled by the RIPK/MLKL axis are representative of neural cell death occurred during AD. Necroptosis causes the release of cellular components, contributing to the pro-inflammatory environment in the AD brain. Inordinately high levels of neural cell death and pro-inflammatory events lead to the production of pro-inflammatory cytokines and feed-forward hyper neuroinflammation. Thus, neural cell death and neuroinflammation cause synaptic dysfunction and memory deficits in the AD brain. In this review, we briefly introduce the mechanisms of neural cell death and neuroinflammation observed in the AD brain. Combined with a typical strategy for targeting Aβ and tau, regulation of neural cell death and neuroinflammation may be effective for the amelioration of AD pathologies. MDPI 2023-07-21 /pmc/articles/PMC10380735/ /pubmed/37511515 http://dx.doi.org/10.3390/ijms241411757 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Choi, Su-Bin
Kwon, Sehee
Kim, Ji-Hye
Ahn, Na-Hyun
Lee, Joo-Hee
Yang, Seung-Hoon
The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title_full The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title_fullStr The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title_full_unstemmed The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title_short The Molecular Mechanisms of Neuroinflammation in Alzheimer’s Disease, the Consequence of Neural Cell Death
title_sort molecular mechanisms of neuroinflammation in alzheimer’s disease, the consequence of neural cell death
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10380735/
https://www.ncbi.nlm.nih.gov/pubmed/37511515
http://dx.doi.org/10.3390/ijms241411757
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