LEXINGTON, KY (August 3, 1998) -- A team of University of Kentucky Chandler Medical Center researchers has recently discovered that Par-4, a protein, may lead to nerve cell death in Alzheimer's disease and related brain disorders. Announced in the August issue of Nature Medicine, the research results show an increased level of the protein -- Par-4 -- in nerve cells in the brains of Alzheimer's disease patients, suggesting the protein may be a contributing factor to the disease.
Blocking Par-4 might be useful as a future treatment for the disease, said Mark Mattson, Ph.D., UK professor of anatomy and neurobiology. "The study's findings identify a new molecular target upon which to aim the emerging arsenal of weapons in the battle against Alzheimer's disease," Mattson said.
Par-4 may play a critical role in nerve cell death in Alzheimer's disease and related brain disorders. Cell death is a fundamental problem in age-related neurodegenerative disorders -- in Alzheimer's disease, nerve cells critical for learning and memory die.
Previous studies have shown that nerve cells in the brains of Alzheimer's patients die by apoptosis, a term used to describe programmed cell death. During the process of apoptosis, a cell shrinks and its DNA (string-like molecules that make up genes) becomes broken into small pieces. Each gene in DNA carries the information required to produce one specific protein. When the gene is expressed, or "switched on," the protein is made. During apoptosis, genes are activated that encode "killer proteins," and these proteins signal cells to begin dying.
The identity of the "killer proteins" and their place in the cascade of events leading to cell death has been a mystery to scientists for decades. The current research may fill one more piece in the puzzle.
Vivek Rangnekar, Ph.D., associate professor of microbiology and
immunology, UK College of Medicine, discovered the gene that codes for Par-4 in
Contact: Kim Cumbie
University of Kentucky Medical Center