Giving the search for Alzheimer's therapies a shot in the arm, researchers have identified the steps that a molecule takes to protect the brain from toxic effects of protein fragments known as amyloid beta, a hallmark of the progressive brain disorder.
"Our discovery centers on a protein called WAVE1, which we found to be important in the production of amyloid beta," said study author Paul Greengard, professor at Rockefeller University in New York.
"The reduction of WAVE1 appears to have a protective effect against the disease," Greengard noted.
Brain cells themselves make amyloid beta, and for reasons that are not fully understood, its accumulation ultimately contributes to the memory loss, personality changes, and other symptoms that patients with this degenerative disease often suffer from.
"When levels of amyloid beta rise, there is an accompanying increase in another molecule, AICD, which reduces the expression of WAVE1. This has the effect of reducing the production of amyloid beta," Greengard explained.
"By targeting steps within this newly discovered pathway, it may be possible to develop drugs to reduce amyloid beta that potentially could be used to either treat or prevent Alzheimer's disease," Greengard pointed out.
WAVE1 is known to help to build filaments of a protein called actin that serve as basic components of cellular structures.
In the current study, the team, examined the levels of WAVE1 in mouse and cellular models of Alzheimer's disease.
They found a dose-dependent response: Mice brains with low WAVE1 levels produced less amyloid-?, and these animals performed better on memory tests.
The study appeared in the journal Nature Medicine.
