More than six million Americans are affected by Alzheimer's disease, a form of dementia marked by accumulation of amyloid-β within the brain. Amyloid-β is a relatively small protein that forms toxic plaques in the brain contributing to the harmful effects of Alzheimer's disease. Another protein, hyperphosphorylated tau (pTau), also accumulates as toxic neurofibrillary tangles.
Together, amyloid-β plaques and pTau tangles result in brain damage, neuroinflammation and ultimately brain death. Gene expression studies have already identified changes in the accumulation of RNA in the brain associated with the development of Alzheimer's disease. However, the full spectrum of gene expression regulation associated with many neurodegenerative diseases, including Alzheimer's, is still not well understood.
To further uncover mechanisms that regulate gene expression in Alzheimer's disease, the National Institutes of Health-National Institute on Aging recently awarded a two-year, $310,000 grant to Petar Grozdanov, Ph.D., from the TTUHSC School of Medicine and Graduate School of Biomedical Sciences.
Grozdanov, an assistant professor in the TTUHSC Department of Cell Biology and Biochemistry, will investigate how perturbed gene expression in the brain can contribute to neurodegenerative disorders like Alzheimer's disease. Specifically, Grozdanov's study will focus on alternative polyadenylation as a molecular mechanism that further regulates protein expression in the brain during the devel.
