Potential target identified for developing new Alzheimer's treatment
University of Minnesota Medical School researchers identified a potential target for treating Alzheimer’s disease, which reversed memory loss in mice. The study could translate to new treatments and provides insight into what may be causing the disease.
The research is published in the current issue of Nature Medicine.
“We’ve identified a target that could be utilized to develop new treatments to restore communication between neurons within the brain,” said Karen Ashe, M.D., Ph.D., professor in the Department of Neurology and senior author of the study. Ashe is also the Founding Director of the N. Bud Grossman Center for Memory Research and Care. Xiaohui Zhao, Ph.D., a research associate in the Ashe lab, led the research.
Ashe’s team looked for a mechanism that could be affecting tau, a protein believed to contribute to cell death and memory impairment. Tau is normal and healthy for the body, but in Alzheimer’s patients, it changes, and clumps together irregularly, causing memory loss. The study was conducted using a mouse model.
Ashe’s team examined several possible causes and found that caspase-2, a naturally-occurring enzyme, may be the culprit. Researchers also discovered tau accumulates in neurons when caspase-2 cleaves, or cuts, healthy tau at a particular point.
By reducing caspase-2, or preventing caspase-2 from cutting tau entirely, recovery of memory deficits could be possible. It’s possible an intervention could even restore cognition.
“This is a significant step forward in the fight against Alzheimer’s disease and memory loss,” Ashe said. “Next, we hope to collaborate with our colleagues in drug development to translate this towards care, with the hope to help improve and preserve the quality of life for those struggling with memory-related conditions.”
Several other University of Minnesota researchers were co-authors of the study including Linda Kotilinek, Benjamin Smith, Chris Hlynialuk, Kathleen Zahs, Martin Ramsden and James Cleary.
Sources of funding for this study include the US National Institutes of Health (NIH) (EUREKA grant no. R01-NS63214 (K.H.A.) and R01-NS79374 (K.H.A.)), the T. and P. Grossman Family Foundation (K.H.A.), B. Grossman (K.H.A.) and K. Moe (K.H.A.).