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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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Dades bibliogràfiques
Publicat a:Mol Neurodegener
Autors principals: Bosson, Anthony, Paumier, Adrien, Boisseau, Sylvie, Jacquier-Sarlin, Muriel, Buisson, Alain, Albrieux, Mireille
Format: Artigo
Idioma:Inglês
Publicat: BioMed Central 2017
Matèries:
Accés en línia: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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