The development of the transgenic mouse is described in the Oct. 4,
1996, Science. Karen Hsiao, M.D., Ph.D., University of Minnesota, led a
team of scientists from the Veterans Administration Medical Center,
Sepulveda, Calif., the Mayo Clinic Jacksonville, Fla., and other
institutions. The National Institute on Aging (NIA) and the National
Institute of Neurological Disorders and Stroke (NINDS), both parts of the
National Institutes of Health, supported the work along with the Alzheimer's
Early in life, the transgenic mice appeared normal. But later, at
9-10 months, the mice had considerable difficulty in a number of memory
tasks when compared with a control group of similarly trained mice. The
oldest trangenics also had between 5 and 14 times the amount of A-Beta peptides associated with amyloid plaques as the younger, normal mice.
For years, scientists have been in disagreement as to whether the
amyloid plaques cause Alzheimer's disease or whether they are a by-product
of some other process. "This is the first animal model to show that amyloid
and deficits in learning and memory are associated," says
D. Stephen Snyder, Ph.D., Program Director, Etiology of Alzheimer's Disease,
NIA. "However, whether the deficits are caused by or merely correlate with
the presence of amyloid remains unresolved. Further testing with this model
may help us understand the relationship between plaques and behavior,
something we need to know for the development of effective drug therapies."
To discuss the findings with NIH scientists, please contact the NIA or
NINDS information offices.