A β 42 and A β 40: similarities and differences
Abstract
The abnormal accumulation of amyloid-β (Aβ) peptide in the brain is one of the most important hallmarks of Alzheimer's disease. Aβ is an aggregation-prone and toxic polypeptide with 39-43 residues, derived from the amyloid precursor protein proteolysis process. According to the amyloid hypothesis, abnormal accumulation of Aβ in the brain is the primary influence driving Alzheimer's disease pathologies. Among all kinds of Aβ isoforms, Aβ40 and Aβ42 are believed to be the most important ones. Although these two kinds of Aβ differ only in two amino acid residues, recent studies show that they differ significantly in their metabolism, physiological functions, toxicities, and aggregation mechanism. In this review, we mainly summarize the similarities and differences between Aβ42 and Aβ40, recent studies on selective inhibitors as well as probes will also be mentioned.
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Aβ42 presents higher cellular toxicity, more aggregation capacity, and a more direct relation with AD pathology.
“This alloform presents higher cellular toxicity, more aggregation capacity, and a more direct relation with AD pathology (Qiu et al., 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Qiu et al., 2015
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References 81 · Cited by 180
- Authors
- Qiu, T., Liu, Q., Chen, Y., Zhao, Y., & Li, Y.
- Affiliations
- Tsinghua University (CN)
- Key Laboratory of Bioorganic Phosphorus Chemistry and Chemical Biology (Ministry of Education), Department of Chemistry Tsinghua University Beijing 100084 China
- Corresponding author
- Chen, Yong‐Xiang
- Venue
- Journal of Peptide Science
- Publisher
- Wiley
- Published
- 2015-05-28
- Volume
- 21
- Issue
- 7
- Pages
- 522-529
- ISSN
- 1075-2617 (ISSN-L)
- 1099-1387
- OpenAlex
- W1750598644
- Cited by
- 180
- References
- 81
- Citations by year
- 2026: 14 · 2025: 16 · 2024: 28 · 2023: 30 · 2022: 26 · 2021: 18 · 2020: 15 · 2019: 11 · 2018: 4 · 2017: 12 · 2016: 5 · 2015: 1
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Peptide Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (21261130090, 21472109)
- Ministry of Science and Technology of the People's Republic of China (2013CB910700, 2012CB821600)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta 42, Aβ40, Alzheimer's disease, amyloid hypothesis, amyloid precursor protein, amyloid fibril formation, amyloid toxicity, amyloid metabolism, selective inhibitors
- MeSH terms
- Alzheimer Disease, Amino Acid Sequence, Antibodies, Monoclonal, Brain Chemistry, Humans, Molecular Sequence Data, Peptide Fragments, Styrenes, Thiazoles, Molecular Probes, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Protein Structure, Secondary, Proteolysis, Protein Aggregation, Pathological
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