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University Of Kentucky Chandler Medical Center Researchers Identify Protein That,,May Cause Nerve Cell Death In Alzheimer's Disease

the neurons were resistant to being killed by amyloid-beta protein and showed lower levels of free radicals.

Other survival-promoting proteins in brain cells, called nerve growth factors, previously were shown to suppress free radical accumulation. They also helped stabilize calcium levels.

Nerve cells were deprived of these growth factors in the present study. Levels of Par-4 rapidly increased, the cells underwent apoptosis, then died. When Par-4 was blocked and the cells were deprived of growth factors, the cells lived, as was the case with the amyloid-beta protein.

Taking their case one step further, researchers then introduced a defective human presenilin-1 gene into cell cultures. People who inherit this defective gene develop Alzheimer's disease at a very early age. Presenilin-1 mutations appear to make nerve cells vulnerable to age-related changes in the brain, such as increased levels of amyloid-beta protein, oxidative stress (a state of damage caused by reactive, oxygen-containing chemicals that can affect a single molecule or an entire organism) and reduced energy availability.

The cell cultures that had the presenilin-1 mutations exhibited increased Par-4 levels following exposure to amyloid-beta protein. More important, however, the team found that blocking Par-4 expression counteracted the adverse effects of the presenilin-1 mutations.

"These findings suggest that Par-4 plays an important role in both the rare early-onset inherited forms of Alzheimer's disease and in the more common sporadic late-onset forms of the disease," Mattson said.

Future investigations may demonstrate the role of Par-4 in other disorders, including epilepsy, amyotrophic lateral sclerosis, Parkinson's disease and stroke. Researchers are also introducing the human Par-4 gene into fertilized mouse eggs. They hope to produce mice with propensities toward cancer and neurodegenerative disorders. These mouse models wou
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Contact: Kim Cumbie
krcumb0@pop.uky.edu
(606) 323-6363
University of Kentucky Medical Center
4-Aug-1998


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