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

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

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The physiological functions of endogenous amyloid-β(Aβ),which plays important role in the pathol-ogy 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 char-acters of Aβ under both physiological and pathological con-ditions.Some worthy studies have shown that the depriva-tion 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 pathophysiol-ogy from the perspective of physiological meaning.

AβPhysiological roleSynapseLTPSynaptic vesicle cycleCognitionAD

Wenwen Cai、Linxi Li、Shaoming Sang、Xiaoli Pan、Chunjiu Zhong

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Department of Neurology,Zhongshan Hospital,Fudan University,Shanghai 200032,China

Basic Medical College,Nanchang University,Nanchang 330031,China

State Key Laboratory of Medical Neurobiology,Institutes of Brain Science & Collaborative Innovation Center for Brain Science,Fudan University,Shanghai 200032,China

Shanghai Municipal Science and Technology Major ProjectNational Key Research and Development Program Foundation of ChinaNational Natural Science Foundation of ChinaNational Natural Science Foundation of ChinaNational Natural Science Foundation of ChinaNational Natural Science Foundation of ChinaNational Natural Science Foundation of ChinaNational Natural Science Foundation of ChinaNatural Science Foundation of Fujian Province

2016YFC13064038187082291332201819010818160093082171408821714112020CXB049

2023

10.1007/s12264-022-00985-9

神经科学通报(英文版)
中国科学院上海生命科学研究院

神经科学通报(英文版)

CSTPCDCSCD
影响因子：0.741
ISSN：1673-7067
年,卷(期)：2023.39(8)
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