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

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Journal Neurosci Bull
Specialty Neurology
Date 2022 Nov 28
PMID 36443453
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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.

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References
1.
Chan K, Wu J, Liu L, Theodoratou E, Car J, Middleton L . Epidemiology of Alzheimer's disease and other forms of dementia in China, 1990-2010: a systematic review and analysis. Lancet. 2013; 381(9882):2016-23. DOI: 10.1016/S0140-6736(13)60221-4. View

2.
Knopman D, Amieva H, Petersen R, Chetelat G, Holtzman D, Hyman B . Alzheimer disease. Nat Rev Dis Primers. 2021; 7(1):33. PMC: 8574196. DOI: 10.1038/s41572-021-00269-y. View

3.
Panza F, Lozupone M, Logroscino G, Imbimbo B . A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease. Nat Rev Neurol. 2019; 15(2):73-88. DOI: 10.1038/s41582-018-0116-6. View

4.
Musiek E, Gomez-Isla T, Holtzman D . Aducanumab for Alzheimer disease: the amyloid hypothesis moves from bench to bedside. J Clin Invest. 2021; 131(20). PMC: 8516468. DOI: 10.1172/JCI154889. View

5.
Kamenetz F, Tomita T, Hsieh H, Seabrook G, Borchelt D, Iwatsubo T . APP processing and synaptic function. Neuron. 2003; 37(6):925-37. DOI: 10.1016/s0896-6273(03)00124-7. View