Telomerase,
an enzyme believed to have a role in determining the life span of
cells, also may protect nerve cells against decreased function and
premature death caused by Alzheimer's disease and other age-related
neurological disorders, according to Mark Mattson, Ph.D., chief of
the Laboratory of Neurosciences at the National Institute on Aging
Gerontology Research Center in Baltimore.
In experiments
designed to mimic conditions in neurologically impaired brains, Mattson
and his colleagues at the NIA and the Sanders-Brown Research Center
on Aging at the University of Kentucky Medical Center in Lexington
found that nerve cells with low levels of telomerase were particularly
vulnerable to being killed by amyloid peptide, a toxic protein that
accumulates in the brains of people with Alzheimer's disease. In contrast,
nerve cells with high levels of telomerase displayed a remarkable
resistance to being damaged or killed in experimental models of Alzheimer's
disease or stroke. The researchers have found that telomerase blocks
a biochemical cascade of reactions called apoptosis, which causes
nerve cells to self-destruct. Accumulating evidence implicates the
process of apoptosis in the death of nerve cells that occurs in Alzheimer's
disease, Parkinson's disease and stroke.
If scientists
can develop methods to stimulate the production of telomerase in nerve
cells, Dr. Mattson said, it might help fend off age-related neurological
disorders.
This
research will be published in the June 2, 2000 issue of the Journal
of Molecular Neuroscience. Further details on Dr. Mattson's telomerase
research will be published in the July issue of the Journal of Neurochemistry,
which will be available after June 15.
