While aging brains of apparently healthy people contain scattered amyloid plaques, the brains of AD patients are littered with them. While aging brains of apparently healthy people contain scattered amyloid plaques, the brains of AD patients are littered with them. Last year, five research groups cloned the gene for the enzyme, called beta-secretase, but the Hopkins scientists say they are the first to show the enzyme is responsible for forming the molecules that comprise plaque within the brain's nerve cells. Beta-secretase is a topic of intense research interest for pharmaceutical and academic centers worldwide because it's one of two enzymes associated with plaque formation.
Many scientists believe plaques are the probable trigger of AD's destruction in the brain.
The research is scheduled for presentation at this year's meetings of the Society for Neuroscience in New Orleans. In the Hopkins study, scientists knocked out the genes for beta-secretase in mice. They then cultured nerve cells from the animals' brains and, using antibodies targeted to beta-secretase, confirmed the enzyme wasn't present. As expected, the nerve cells lacking the enzyme failed to form beta amyloid, the plaque protein. Last year, other researchers reported preventing plaque production in mice by immunizing the animals against their own plaque protein.