TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide
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DOI: 10.1186/s13024-017-0194-8
Abstract: BackgroundExcessive 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.… read more here.
Keywords: hyperactivity; synaptic dysfunction; trpa1 channels; ca2 hyperactivity ... See more keywords