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Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?

Alzheimer’s disease (AD) is one of the most common causes of dementia. Its pathogenesis is characterized by the aggregation of the amyloid-β (Aβ) protein in senile plaques and the hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Current medications for AD can provide temporar...

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Detalles Bibliográficos
Autores principales: Dong, Yuan, Li, Xiaoheng, Cheng, Jinbo, Hou, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386861/
https://www.ncbi.nlm.nih.gov/pubmed/30696107
http://dx.doi.org/10.3390/ijms20030558
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author Dong, Yuan
Li, Xiaoheng
Cheng, Jinbo
Hou, Lin
author_facet Dong, Yuan
Li, Xiaoheng
Cheng, Jinbo
Hou, Lin
author_sort Dong, Yuan
collection PubMed
description Alzheimer’s disease (AD) is one of the most common causes of dementia. Its pathogenesis is characterized by the aggregation of the amyloid-β (Aβ) protein in senile plaques and the hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Current medications for AD can provide temporary help with the memory symptoms and other cognitive changes of patients, however, they are not able to stop or reverse the progression of AD. New medication discovery and the development of a cure for AD is urgently in need. In this review, we summarized drugs for AD treatments and their recent updates, and discussed the potential of microglia induced neuroinflammation as a target for anti-AD drug development.
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spelling pubmed-63868612019-02-27 Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target? Dong, Yuan Li, Xiaoheng Cheng, Jinbo Hou, Lin Int J Mol Sci Review Alzheimer’s disease (AD) is one of the most common causes of dementia. Its pathogenesis is characterized by the aggregation of the amyloid-β (Aβ) protein in senile plaques and the hyperphosphorylated tau protein in neurofibrillary tangles in the brain. Current medications for AD can provide temporary help with the memory symptoms and other cognitive changes of patients, however, they are not able to stop or reverse the progression of AD. New medication discovery and the development of a cure for AD is urgently in need. In this review, we summarized drugs for AD treatments and their recent updates, and discussed the potential of microglia induced neuroinflammation as a target for anti-AD drug development. MDPI 2019-01-28 /pmc/articles/PMC6386861/ /pubmed/30696107 http://dx.doi.org/10.3390/ijms20030558 Text en © 2019 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Dong, Yuan
Li, Xiaoheng
Cheng, Jinbo
Hou, Lin
Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title_full Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title_fullStr Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title_full_unstemmed Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title_short Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?
title_sort drug development for alzheimer’s disease: microglia induced neuroinflammation as a target?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386861/
https://www.ncbi.nlm.nih.gov/pubmed/30696107
http://dx.doi.org/10.3390/ijms20030558
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