April 3, 2001 - A laboratory "fishing expedition" landed a surprising catch for researchers: a cholesterol-lowering protein produced by the body that might be able to slow the progression of Alzheimer's disease.

The findings are reported in the current (March 27) issue of Biochemistry, a peer-reviewed journal of the American Chemical Society, the world's largest scientific society.

Using a protein implicated in Alzheimer's disease - amyloid precursor protein - for bait, University of Pittsburgh researchers trolled a "lake" of chemicals specifically designed to simulate the human body to see what might grab their unusual lure. A small part of amyloid precursor protein forms a chemical called beta amyloid, which becomes the most important part of the Alzheimer's disease plaques that strangle normal brain cells.

The bait eventually produced a bite, another protein called Apolipoprotein A-1.

Everyone has some quantity of Apolipoprotein A-1, or Apo-A, in their body, says Dr. Radosveta Koldamova, M.D., Ph.D., a member of the research team. It is produced in the small intestine and the liver and is known to help prevent coronary heart disease. At normal levels, the protein clears cholesterol throughout the body, including in the brain. The scientists speculate that boosting Apo-A levels may also help clear beta amyloid.

The researchers think that increasing the concentrations of Apo-A in blood might delay the dementia associated with Alzheimer's disease. Further testing is needed to confirm their hypothesis, they add. Another such protein, Apolipoprotein E, has been similarly linked with Alzheimer's and is being studied by other researchers.

"You begin to think about whether or not changing Apo-A levels in the blood could benefit Alzheimer's patients," Koldamova said.

One way to raise the levels of the protein naturally is through a good diet, according to Professor John S. Lazo, Ph.D., who led the research study. Previous findings indicate
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Contact: Beverly Hassell
b_hassell@acs.org
202-872-4065
American Chemical Society
1-Apr-2001