Scientists Develop Mouse Model for Alzheimer’s Disease

A new mouse model that will further understanding of Alzheimer’s disease and ultimately allow for testing of drug therapies has been developed by scientists at the University of Minnesota. The genetically-engineered mouse is the first to exhibit both behavioral characteristics of Alzheimer’s dementia and protein-derived plaques like those which appear in the brains of people with Alzheimer’s disease.

Findings and Implications

The development of the transgenic mouse is described in the October 4, 1996, Science. Karen Hsiao, M.D., Ph.D., University of Minnesota, led a team of scientists from the Veterans Administration Medical Center, Sepulveda, California; the Mayo Clinic Jacksonville, Florida; 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 Association.

Early in life, the transgenic mouse 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 transgenics 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 byproduct 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.”


National Institute on Aging

Press Release

October 3, 1996

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