Enzyme May Be a Key to Alzheimer's Disease

A specific enzyme known as BACE1 (beta-site amyloid precursor protein cleaving enzyme1) has been found in mice studies to be one of the essential elements in the development of amyloid plaques that collect and surround brain cells causing Alzheimer's disease, according to researchers at Johns Hopkins University School of Medicine.

This discovery shows that blocking the enzyme may be an avenue to prevention of the disease, according to researchers.

"Knowing this enzyme is the major player in forming plaques offers a way to tell if the structures truly are important in Alzheimer's. And if that's the case, the enzyme also offers a clear target for therapy," said Dr. Philip Wong, lead neuroscientist at Johns Hopkins.

The protein deposits, amyloid plaques, are formed when two enzymes, BACE 1 and BACE 2, trim a molecule called amyloid precursor protein (APP) into smaller pieces. Researchers found that mice lacking BACE1 do not generate the protein pieces seen in the amyloid plaques, according to the research published in Nature Neuroscience.

"We're really encouraged by possible therapeutic implications," said Wong. "Scientists are already screening for compounds that block the action of beta-secretase in hopes of designing small molecules able to cross the brain's blood-brain barrier."

The molecules could be fine-tuned to inhibit beta-secretase, said Wong, which would halt plaque production.

Other sources: Johns Hopkins, Reuters