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Hopkins scientists show enzyme is key to hallmark of Alzheimer's

ouraged by possible therapeutic implications," says Wong, "because scientists are already designing small molecules capable of crossing the brain's blood-brain barrier." The molecules could, in theory, be fine-tuned to inhibit such enzymes as beta-secretase, Wong adds, which could squelch plaque production.

Last year, other researchers reported preventing plaque production in mice by immunizing the animals against their own plaque protein. "Both approaches may prove useful in treating Alzheimer's," Wong explains.

Beta-secretase works by trimming pieces off a larger molecule that's parent to the plaque protein, beta amyloid. Forming amyloid is a natural cell process, says Wong. It's part of a poorly understood event in cells where amyloid appears and then is cleared. "But in Alzheimer's," he explains, "something goes wrong and amyloid really increases."

A current hypothesis of AD is that as amyloid builds up, nerve cells are damaged and brain tissues become inflamed. Some researchers believe this chronic inflammation progressively injures nerve cells, leading to the symptoms of the disease.

Scientists say another enzyme, called gamma-secretase, is also involved in brain production of plaque. However, the Hopkins researchers say, the nature of gamma-secretase remains controversial.

Gamma-secretase is a research hot spot because nearly a quarter of the people with early-onset Alzheimer's have mutations in genes (presenilin genes) linked with the enzyme's activity.


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Contact: Marjorie Centofanti
mcentofanti@jhmi.edu
410-955-8725
Johns Hopkins Medical Institutions
5-Nov-2000


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