TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

Abstract Background Excessive synaptic loss is thought to be one of the earliest events in Alzheimer’s disease (AD). However, the key mechanisms that maintain plasticity of synapses during adulthood or initiate synapse dysfunction in AD remain unknown. Recent studies suggest that astrocytes contribu...

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Bibliographic Details
Main Authors: Anthony Bosson, Adrien Paumier, Sylvie Boisseau, Muriel Jacquier-Sarlin, Alain Buisson, Mireille Albrieux
Format: Article
Language:English
Published: BMC 2017-07-01
Series:Molecular Neurodegeneration
Subjects:
Online Access:http://link.springer.com/article/10.1186/s13024-017-0194-8