TRPA1 channels promote astrocytic Ca(2+) hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

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 contribute to fu...

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Bibliografiska uppgifter
I publikationen:Mol Neurodegener
Huvudupphovsmän: Bosson, Anthony, Paumier, Adrien, Boisseau, Sylvie, Jacquier-Sarlin, Muriel, Buisson, Alain, Albrieux, Mireille
Materialtyp: Artigo
Språk:Inglês
Publicerad: BioMed Central 2017
Ämnen:
Research Article
Länkar:https://ncbi.nlm.nih.gov/pmc/articles/PMC5501536/
https://ncbi.nlm.nih.gov/pubmed/28683776
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/s13024-017-0194-8
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