Article
Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses.
Neurobiology of disease - 1 Nov 2005
Almeida Claudia G, Tampellini Davide, Takahashi Reisuke H, Greengard Paul, Lin Michael T, Snyder Eric M, Gouras Gunnar K
Abstract excerpt
Synaptic dysfunction is increasingly viewed as an early manifestation of Alzheimer's disease (AD), but the cellular mechanism by which beta-amyloid (Abeta) may affect synapses remains unclear. Since cultured neurons derived from APP mutant transgenic mice secrete elevated levels of Abeta and parallel the subcellular Abeta accumulation seen in vivo, we asked whether alterations in synapses occur in this setting....
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
