The Toxicity and Polymorphism of β-Amyloid Oligomers

It is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of Alzheimer’s disease (AD) by inducing neuron damage and cognitive impairment, but Aβos are highly heterogeneous in their size, structure and cytotoxicity, making the corresponding studies tough to carry out. N...

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Main Authors: Ya-ru Huang, Rui-tian Liu
Format: Article
Language:English
Published: MDPI AG 2020-06-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/21/12/4477
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spelling doaj-c79b52295e6d4658945606223e30dd852020-11-25T01:20:26ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-06-01214477447710.3390/ijms21124477The Toxicity and Polymorphism of β-Amyloid OligomersYa-ru Huang0Rui-tian Liu1State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, ChinaState Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, ChinaIt is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of Alzheimer’s disease (AD) by inducing neuron damage and cognitive impairment, but Aβos are highly heterogeneous in their size, structure and cytotoxicity, making the corresponding studies tough to carry out. Nevertheless, a number of studies have recently made remarkable progress in the describing the characteristics and pathogenicity of Aβos. We here review the mechanisms by which Aβos exert their neuropathogenesis for AD progression, including receptor binding, cell membrane destruction, mitochondrial damage, Ca<sup>2+</sup> homeostasis dysregulation and tau pathological induction. We also summarize the characteristics and pathogenicity such as the size, morphology and cytotoxicity of dimers, trimers, Aβ*56 and spherical oligomers, and suggest that Aβos may play a different role at different phases of AD pathogenesis, resulting in differential consequences on neuronal synaptotoxicity and survival. It is warranted to investigate the temporal sequence of Aβos in AD human brain and examine the relationship between different Aβos and cognitive impairment.https://www.mdpi.com/1422-0067/21/12/4477β-amyloid oligomersAlzheimer’s diseasepolymorphismtoxicityaggregation
collection DOAJ
language English
format Article
sources DOAJ
author Ya-ru Huang
Rui-tian Liu
spellingShingle Ya-ru Huang
Rui-tian Liu
The Toxicity and Polymorphism of β-Amyloid Oligomers
International Journal of Molecular Sciences
β-amyloid oligomers
Alzheimer’s disease
polymorphism
toxicity
aggregation
author_facet Ya-ru Huang
Rui-tian Liu
author_sort Ya-ru Huang
title The Toxicity and Polymorphism of β-Amyloid Oligomers
title_short The Toxicity and Polymorphism of β-Amyloid Oligomers
title_full The Toxicity and Polymorphism of β-Amyloid Oligomers
title_fullStr The Toxicity and Polymorphism of β-Amyloid Oligomers
title_full_unstemmed The Toxicity and Polymorphism of β-Amyloid Oligomers
title_sort toxicity and polymorphism of β-amyloid oligomers
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1661-6596
1422-0067
publishDate 2020-06-01
description It is widely accepted that β-amyloid oligomers (Aβos) play a key role in the progression of Alzheimer’s disease (AD) by inducing neuron damage and cognitive impairment, but Aβos are highly heterogeneous in their size, structure and cytotoxicity, making the corresponding studies tough to carry out. Nevertheless, a number of studies have recently made remarkable progress in the describing the characteristics and pathogenicity of Aβos. We here review the mechanisms by which Aβos exert their neuropathogenesis for AD progression, including receptor binding, cell membrane destruction, mitochondrial damage, Ca<sup>2+</sup> homeostasis dysregulation and tau pathological induction. We also summarize the characteristics and pathogenicity such as the size, morphology and cytotoxicity of dimers, trimers, Aβ*56 and spherical oligomers, and suggest that Aβos may play a different role at different phases of AD pathogenesis, resulting in differential consequences on neuronal synaptotoxicity and survival. It is warranted to investigate the temporal sequence of Aβos in AD human brain and examine the relationship between different Aβos and cognitive impairment.
topic β-amyloid oligomers
Alzheimer’s disease
polymorphism
toxicity
aggregation
url https://www.mdpi.com/1422-0067/21/12/4477
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