Synaptic Damage In Alzheimer Disease

An abnormal protein fragment, dubbed "Abeta", is suspected to be pivotal in the disease process because all the genetic mutations that cause the disease increase its accumulation. The catch is that accumulation of this protein in cellular aggregates does not correlate well with the timing or severity of symptoms. Researchers have proposed that symptoms may instead relate to accumulation of Abeta at synapses, the connections between neurons, because cognitive decline does correlate with synapse loss. Now, Paul

Greengard and colleagues report that Abeta triggers a cellular mechanism that removes so-called NMDA receptors from the cell surface in mutant mice, which express a protein that causes Alzheimer disease in humans. These receptors are essential for adjusting the strength of signals between nerve cells. When their levels decline, connections between nerve cells cannot be strengthened, as they usually are when we learn something. If these findings are confirmed in humans, they might provide a link between the Abeta fragment and memory loss in Alzheimer disease.

Author contact:
Eric M. Snyder
Email: ericmaltesnyder@gmail.com

Additional contact for comment on paper:
Rudolph Tanzi (Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA)
E-mail: tanzi@helix.mgh.harvard.edu

lso published online.

(C) Nature Neuroscience press release.

Message posted by: Trevor M. D'Souza