Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.
10.1007/s12264-022-00985-9
- Author:
Wenwen CAI
1
;
Linxi LI
2
;
Shaoming SANG
1
;
Xiaoli PAN
3
;
Chunjiu ZHONG
4
Author Information
1. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
2. Basic Medical College, Nanchang University, Nanchang, 330031, China.
3. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. panxiaoli0708@126.com.
4. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. zhongcj@163.com.
- Publication Type:Review
- Keywords:
AD;
Aβ;
Cognition;
LTP;
Physiological role;
Synapse;
Synaptic vesicle cycle
- MeSH:
Humans;
Alzheimer Disease/pathology*;
Amyloid beta-Peptides/metabolism*;
Long-Term Potentiation;
Synaptic Transmission/physiology*;
Hippocampus
- From:
Neuroscience Bulletin
2023;39(8):1289-1308
- CountryChina
- Language:English
-
Abstract:
The physiological functions of endogenous amyloid-β (Aβ), which plays important role in the pathology of Alzheimer's disease (AD), have not been paid enough attention. Here, we review the multiple physiological effects of Aβ, particularly in regulating synaptic transmission, and the possible mechanisms, in order to decipher the real characters of Aβ under both physiological and pathological conditions. Some worthy studies have shown that the deprivation of endogenous Aβ gives rise to synaptic dysfunction and cognitive deficiency, while the moderate elevation of this peptide enhances long term potentiation and leads to neuronal hyperexcitability. In this review, we provide a new view for understanding the role of Aβ in AD pathophysiology from the perspective of physiological meaning.
