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Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease

Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases in the world, which is characterized by memory dysfunction and the formation of tau and amyloid β (Aβ) aggregates in multiple brain regions, including the hippocampus and cortex. The formation of senile plaques involvi...

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Autores principales: Rahman, Md. Ataur, Rahman, MD. Hasanur, Mamun-Or-Rashid, A. N. M., Hwang, Hongik, Chung, Sooyoung, Kim, Bonglee, Rhim, Hyewhon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138936/
https://www.ncbi.nlm.nih.gov/pubmed/35625764
http://dx.doi.org/10.3390/biomedicines10051027
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author Rahman, Md. Ataur
Rahman, MD. Hasanur
Mamun-Or-Rashid, A. N. M.
Hwang, Hongik
Chung, Sooyoung
Kim, Bonglee
Rhim, Hyewhon
author_facet Rahman, Md. Ataur
Rahman, MD. Hasanur
Mamun-Or-Rashid, A. N. M.
Hwang, Hongik
Chung, Sooyoung
Kim, Bonglee
Rhim, Hyewhon
author_sort Rahman, Md. Ataur
collection PubMed
description Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases in the world, which is characterized by memory dysfunction and the formation of tau and amyloid β (Aβ) aggregates in multiple brain regions, including the hippocampus and cortex. The formation of senile plaques involving tau hyperphosphorylation, fibrillar Aβ, and neurofibrillary tangles (NFTs) is used as a pathological marker of AD and eventually produces aggregation or misfolded protein. Importantly, it has been found that the failure to degrade these aggregate-prone proteins leads to pathological consequences, such as synaptic impairment, cytotoxicity, neuronal atrophy, and memory deficits associated with AD. Recently, increasing evidence has suggested that the autophagy pathway plays a role as a central cellular protection system to prevent the toxicity induced by aggregation or misfolded proteins. Moreover, it has also been revealed that AD-related protein aggresomes could be selectively degraded by autophagosome and lysosomal fusion through the autophagy pathway, which is known as aggrephagy. Therefore, the regulation of autophagy serve as a useful approach to modulate the formation of aggresomes associated with AD. This review focuses on the recent improvements in the application of natural compounds and small molecules as a potential therapeutic approach for AD prevention and treatment via aggrephagy.
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spelling pubmed-91389362022-05-28 Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease Rahman, Md. Ataur Rahman, MD. Hasanur Mamun-Or-Rashid, A. N. M. Hwang, Hongik Chung, Sooyoung Kim, Bonglee Rhim, Hyewhon Biomedicines Review Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases in the world, which is characterized by memory dysfunction and the formation of tau and amyloid β (Aβ) aggregates in multiple brain regions, including the hippocampus and cortex. The formation of senile plaques involving tau hyperphosphorylation, fibrillar Aβ, and neurofibrillary tangles (NFTs) is used as a pathological marker of AD and eventually produces aggregation or misfolded protein. Importantly, it has been found that the failure to degrade these aggregate-prone proteins leads to pathological consequences, such as synaptic impairment, cytotoxicity, neuronal atrophy, and memory deficits associated with AD. Recently, increasing evidence has suggested that the autophagy pathway plays a role as a central cellular protection system to prevent the toxicity induced by aggregation or misfolded proteins. Moreover, it has also been revealed that AD-related protein aggresomes could be selectively degraded by autophagosome and lysosomal fusion through the autophagy pathway, which is known as aggrephagy. Therefore, the regulation of autophagy serve as a useful approach to modulate the formation of aggresomes associated with AD. This review focuses on the recent improvements in the application of natural compounds and small molecules as a potential therapeutic approach for AD prevention and treatment via aggrephagy. MDPI 2022-04-29 /pmc/articles/PMC9138936/ /pubmed/35625764 http://dx.doi.org/10.3390/biomedicines10051027 Text en © 2022 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
Rahman, Md. Ataur
Rahman, MD. Hasanur
Mamun-Or-Rashid, A. N. M.
Hwang, Hongik
Chung, Sooyoung
Kim, Bonglee
Rhim, Hyewhon
Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title_full Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title_fullStr Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title_full_unstemmed Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title_short Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer’s Disease
title_sort autophagy modulation in aggresome formation: emerging implications and treatments of alzheimer’s disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138936/
https://www.ncbi.nlm.nih.gov/pubmed/35625764
http://dx.doi.org/10.3390/biomedicines10051027
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