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Open AccessmGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo
NMDA-type glutamate receptors (NMDARs) are currently regarded as paramount in the potent and selective disruption of synaptic plasticity by Alzheimer’s disease amyloid β-protein (Aβ). Non-NMDAR mechanisms rema...
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Open AccessExosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo
Exosomes, small extracellular vesicles of endosomal origin, have been suggested to be involved in both the metabolism and aggregation of Alzheimer’s disease (AD)-associated amyloid β-protein (Aβ). Despite thei...
