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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)...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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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. |
format | Online Article Text |
id | pubmed-10380735 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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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