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Amyloid Beta in Aging and Alzheimer’s Disease
Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in elderly individuals. AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a c...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9655207/ https://www.ncbi.nlm.nih.gov/pubmed/36361714 http://dx.doi.org/10.3390/ijms232112924 |
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author | Sehar, Ujala Rawat, Priyanka Reddy, Arubala P. Kopel, Jonathan Reddy, P. Hemachandra |
author_facet | Sehar, Ujala Rawat, Priyanka Reddy, Arubala P. Kopel, Jonathan Reddy, P. Hemachandra |
author_sort | Sehar, Ujala |
collection | PubMed |
description | Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in elderly individuals. AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a combination of lifestyle, environment and genetic factors causes the late-onset sporadic form of the disease. However, accelerated disease progression is noticed in patients with familial AD. Disease-causing pathological changes are synaptic damage, and mitochondrial structural and functional changes, in addition to increased production and accumulation of phosphorylated tau (p-tau), and amyloid beta (Aβ) in the affected brain regions in AD patients. Aβ is a peptide derived from amyloid precursor protein (APP) by proteolytic cleavage of beta and gamma secretases. APP is a glycoprotein that plays a significant role in maintaining neuronal homeostasis like signaling, neuronal development, and intracellular transport. Aβ is reported to have both protective and toxic effects in neurons. The purpose of our article is to summarize recent developments of Aβ and its association with synapses, mitochondria, microglia, astrocytes, and its interaction with p-tau. Our article also covers the therapeutic strategies that reduce Aβ toxicities in disease progression and discusses the reasons for the failures of Aβ therapeutics. |
format | Online Article Text |
id | pubmed-9655207 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-96552072022-11-15 Amyloid Beta in Aging and Alzheimer’s Disease Sehar, Ujala Rawat, Priyanka Reddy, Arubala P. Kopel, Jonathan Reddy, P. Hemachandra Int J Mol Sci Review Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in elderly individuals. AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a combination of lifestyle, environment and genetic factors causes the late-onset sporadic form of the disease. However, accelerated disease progression is noticed in patients with familial AD. Disease-causing pathological changes are synaptic damage, and mitochondrial structural and functional changes, in addition to increased production and accumulation of phosphorylated tau (p-tau), and amyloid beta (Aβ) in the affected brain regions in AD patients. Aβ is a peptide derived from amyloid precursor protein (APP) by proteolytic cleavage of beta and gamma secretases. APP is a glycoprotein that plays a significant role in maintaining neuronal homeostasis like signaling, neuronal development, and intracellular transport. Aβ is reported to have both protective and toxic effects in neurons. The purpose of our article is to summarize recent developments of Aβ and its association with synapses, mitochondria, microglia, astrocytes, and its interaction with p-tau. Our article also covers the therapeutic strategies that reduce Aβ toxicities in disease progression and discusses the reasons for the failures of Aβ therapeutics. MDPI 2022-10-26 /pmc/articles/PMC9655207/ /pubmed/36361714 http://dx.doi.org/10.3390/ijms232112924 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 Sehar, Ujala Rawat, Priyanka Reddy, Arubala P. Kopel, Jonathan Reddy, P. Hemachandra Amyloid Beta in Aging and Alzheimer’s Disease |
title | Amyloid Beta in Aging and Alzheimer’s Disease |
title_full | Amyloid Beta in Aging and Alzheimer’s Disease |
title_fullStr | Amyloid Beta in Aging and Alzheimer’s Disease |
title_full_unstemmed | Amyloid Beta in Aging and Alzheimer’s Disease |
title_short | Amyloid Beta in Aging and Alzheimer’s Disease |
title_sort | amyloid beta in aging and alzheimer’s disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9655207/ https://www.ncbi.nlm.nih.gov/pubmed/36361714 http://dx.doi.org/10.3390/ijms232112924 |
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