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2017 Grants - Caccamo
Molecular Mechanisms of Cognitive Decline in Alzheimer’s Disease
Antonella Caccamo, Ph.D.
Arizona State University
2017 Alzheimer’s Association Research Grant (AARG)
Do alterations in the protein NR4a2 promote memory loss in Alzheimer’s disease?
The build-up of amyloid plaques and tau tangles in the brain is a hallmark of Alzheimer’s disease. However, it is not yet clear how these changes lead to progressive memory loss. The activity of many different genes and proteins is necessary for normal learning and memory processes. In previous studies, Antonella Caccamo, Ph.D., and colleagues found that a protein called NR4a2 (nuclear receptor subfamily-4a2) is activated in the brains of normal mice during learning, but not in Alzheimer’s-like mice. They hypothesize that learning-induced activity of NR4a2 is necessary for proper memory formation, and that lack of this protein could be a contributing factor to cognitive decline in Alzheimer’s disease.
For their current studies, Dr. Caccamo will increase or decrease the levels of NR4a2 in the brains of normal and Alzheimer’s-like mice and measure the effects on their memory function. A main focus will be to increase the activity of NR4a2 in the brains of Alzheimer’s-like mice to see if this can improve their cognition and preserve nerve cell connections. They will also determine how NR4a2 affects the function of other genes and proteins involved in learning and memory processes.
The results of this work could provide new information on the role of NR4a2 in memory formation and Alzheimer’s disease. These findings could also help determine if the development of treatments to increase NR4a2 could potentially slow or prevent cognitive decline associated with Alzheimer’s disease.