Researchers at MUSC, the University of California, San Diego, and American Life Science Pharmaceuticals of San Diego (UCSD) have validated gene cathepsin B (CatB) as a target for improving memory deficits and reducing Alzheimer's disease in animal models representative of most patients with the disease.
The study has been published in the online edition of the Journal of Alzheimer's Disease (Vol. 29, No. 4).
Lead investigator Mark S. Kindy, Ph.D., professor of Neurosciences of the MUSC College of Medicine and career research scientist at the Ralph H. Johnson VA Medical Center, feels the study is important because it could lead to new treatments for improving memory deficits of patients with Alzheimer's disease. Alzheimer's disease is a degenerative and ultimately fatal disorder affecting as many as 5.3 million Americans and an estimated 80,000 South Carolinians, according to the Alzheimer's Association.
Another gene, BACE1, has long been thought to be a cause of the disease because deleting BACE1 from animal models reduces brain plaque, which is the substance responsible for some Alzheimer's disease symptoms. However, deleting the BACE1 gene was reported to make memory deficits significantly worse in animal models.
In the current study, the researchers show that deleting CatB in mouse models improves memory deficits and also reduces plaque.
Co-authors of the study were Gregory Hook, Ph.D., of American Life Science Pharmaceuticals in San Diego, and Vivian Hook, Ph.D., of the UCSD, Jin Yu, M.D., and Hong Zhu, M.D., MUSC; and Salim S. El-Amouri, Ph.D., Cincinnati Children's Hospital Medical Center, University of Cincinnati.
The study was supported in part by grants from the National Institute of Aging of the National Institutes of Health, the Alzheimer's Drug Discovery Foundation and the Alzheimer's Association.