A key aspect in the development of Alzheimer’s disease is the formation of structures called plaques in the brain. Studies have suggested that these plaques form when the protein amyloid beta is converted from a soluble to an insoluble form and takes on a configuration of hair-shaped threads called fibrils. Unable to be cleared out of the brain, the fibrils eventually
cluster together and become the amyloid plaques that are a hallmark of Alzheimer’s.

David M. Holtzman, the Andrew B. and Gretchen P. Jones Professor of Neurology and head of the neurology department, studies the metabolism of amyloid beta in Alzheimer’s disease.

David M. Holtzman, the Andrew B. and Gretchen P. Jones Professor of Neurology and head of the Department of Neurology, studies the metabolism of amyloid beta to try to determine what controls the production and clearance of the protein and how to prevent its buildup in the brain. Scientists believe the buildup of the protein starts 10 to 15 years before disease symptoms appear.

“Determining if the brain’s metabolism of amyloid beta becomes altered during the course of the disease could be used as a way to diagnose when the disease is starting,” Holtzman says. “We think developing antecedent biomarkers for Alzheimer’s is very important. It would be analogous to knowing if a patient is building up cholesterol in coronary arteries and, if so, starting a drug treatment before he or she has a heart attack or stroke.”

Holtzman also is studying antibodies that his lab has demonstrated prevent the toxicity or increase the removal of amyloid beta from the brain. Clinical trials now are being conducted on antibodies, such as these, in humans.

Additionally, in Holtzman’s laboratory, Randy Bateman, assistant professor of neurology, has developed a new technique that can measure the rates of synthesis and clearance of proteins in the central nervous system. This could be useful for discovering new biomarkers for neurodegenerative diseases.

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