Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology

 Wenwen Cai1  · Linxi Li2  · Shaoming Sang1  · Xiaoli Pan1  · Chunjiu Zhong1,3
1 Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032, China 
2 Basic Medical College, Nanchang University, Nanchang 330031, China 
3 State Key Laboratory of Medical Neurobiology, Institutes of Brain Science & Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China

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.

Keywords
Aβ; Physiological role; Synapse; LTP; Synaptic vesicle cycle; Cognition; AD