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Article
Review Article
Exp Neurobiol 2022; 31(2): 65-88
Published online April 30, 2022
https://doi.org/10.5607/en22004
© The Korean Society for Brain and Neural Sciences
Physiological Roles of Monomeric Amyloid-β and Implications for Alzheimer’s Disease Therapeutics
Hyomin Jeong1,2,3†, Heewon Shin2,3†, Seungpyo Hong2,4,5,6 and YoungSoo Kim1,2,3,4*
1Division of Integrated Science and Engineering, Underwood International College, Yonsei University, Incheon 21983, 2Department of Pharmacy and 3Yonsei Institute of Pharmaceutical Sciences, College of Pharmacy, Yonsei University, Incheon 21983, 4Yonsei Frontier Lab, Yonsei University, Seoul 03722, Korea, 5Division of Pharmaceutical Sciences, School of Pharmacy, University of Wisconsin-Madison, Madison, 6Wisconsin Center for NanoBioSystems, University of Wisconsin-Madison, Madison, WI 53705, USA
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-32-749-4523, FAX: 82-32-749-4105
e-mail: y.kim@yonsei.ac.kr
†These authors contributed equally to this article.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Alzheimer’s disease (AD) progressively inflicts impairment of synaptic functions with notable deposition of amyloid-β (Aβ) as senile plaques within the extracellular space of the brain. Accordingly, therapeutic directions for AD have focused on clearing Aβ plaques or preventing amyloidogenesis based on the amyloid cascade hypothesis. However, the emerging evidence suggests that Aβ serves biological roles, which include suppressing microbial infections, regulating synaptic plasticity, promoting recovery after brain injury, sealing leaks in the blood-brain barrier, and possibly inhibiting the proliferation of cancer cells. More importantly, these functions were found in
Graphical Abstract
Keywords: Alzheimer’s disease, Amyloid beta-peptides, Amyloidosis, Neurodegenerative diseases, Therapeutics
