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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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 |
work_keys_str_mv |
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