Brain plaques believed to contribute to Alzheimer's disease melt away in mice when robbed of a key enzyme, researchers report.
And the rodents' intellectual function actually improved as their amyloid plaques dissolved from lack of beta-secretase (BACE1), an enzyme critical in the formation of the plaques, said senior researcher Riqiang Yan. He is vice chair of neuroscience with the Cleveland Clinic Lerner Research Institute.
The investigators had expected that blocking BACE1 would slow or halt the formation of amyloid plaques, but were surprised to find that it also caused existing plaques to fade away, Yan said.
"When we looked at the mice later -- at six months old and 10 months old -- all those pre-existing plaques were gone," Yan said. "Sequential deletion of beta-secretase actually can reverse existing plaques."
These results are good news for companies developing BACE1-inhibitor drugs as a potential treatment for Alzheimer's disease, Yan said. He noted that five such drugs are being tested in clinical trials.