The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses.
Claudia G Almeida; Davide Tampellini; Reisuke H Takahashi; Paul Greengard; Michael T Lin; Eric M Snyder; Gunnar K Gouras (Profiled Author: Greengard, Paul)
Department of Neurology and Neuroscience, Laboratory of Alzheimer's Disease Neurobiology, Weill Medical College of Cornell University, 525 E 68th Street, NY 10021, USA.
Neurobiology of disease 2005;20(2):187-98.
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. We report that cultured Tg2576 APP mutant neurons have selective alterations in pre- and post-synaptic compartments compared to wild-type neurons. Post-synaptic compartments appear fewer in number and smaller, while active pre-synaptic compartments appear fewer in number and enlarged. Among the earliest changes in synaptic composition in APP mutant neurons were reductions in PSD-95, a protein involved in recruiting and anchoring glutamate receptor subunits to the post-synaptic density. In agreement, we observed early reductions in surface expression of glutamate receptor subunit GluR1 in APP mutant neurons. We provide evidence that Abeta is specifically involved in these alterations in synaptic biology, since alterations in PSD-95 and GluR1 are blocked by gamma-secretase inhibition, and since exogenous addition of synthetic Abeta to wild-type neurons parallels changes in synaptic PSD-95 and GluR1 observed in APP mutant neurons.
1 Originating Grant
30 September 1997 - 31 January 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 23,889,772
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
2 September 2011 - 30 June 2014
FOGARTY INTERNATIONAL CENTER
Total Funding: $ 70,352
Golde, Todd E
10 April 2000 - 30 April 2009
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 2,532,291
HYMAN, BRADLEY T
15 April 2011 - 31 March 2016
NATIONAL INSTITUTE ON AGING
Total Funding: $ 868,259
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