Rammohan Rao, PhD

Associate Research Professor
Research Focus

Misfolded Proteins, ER stress-induced cell death and Mechanisms of Neurodegenerative Disease.

Over the past 15 years, we have made extensive contributions to the understanding of neuronal cell death triggered by misfolded proteins.  We have been investigating the mechanisms and biochemical pathways that couple misfolded proteins to the neuronal cell death programs and have published more than a dozen papers and reviews in this area.  Two manuscripts (Rao RV et al J Biol Chem 277 (24): 21836-42, 2002, and Rao RV et al Cell Death & Differ (3):415-25; 2006) received top citations from the F1000 Biology and two manuscripts (Rao RV et al J Biol Chem 276: 33869-33874, 2001 & Rao RV et al J Biol Chem 277: 21836-42, 2002) were placed in the top 1% by Essential Science Indicators in terms of the citations these articles received.

The major genetic risk factor for Alzheimer’s Disease (AD) is the lipid binding and transporting carrier protein Apolipoprotein E, epsilon 4 allele (ApoE4). One of the unsolved mysteries of AD is how ApoE4 triggers this age-associated incurable neurodegenerative disease.  Recently, we showed that ApoE4 is a transcription factor and binds to the promoters of genes involved in a range of processes linked to aging and AD disease pathogenesis. These findings are very exciting as it links for the first time ApoE4-mediated signaling with genes involved in sirtuin function, energy metabolism, inflammation, axon guidance, neuronal survival, and cell death, offering new insight into Alzheimer’s disease pathogenesis. Our work together with our recent publications (Theendakara et al, PNAS 2013;Theendakara et al., 2016; Theendakara et al., 2017) have led to a clearer understanding of the role of ApoE4 as a risk factor for AD, and most importantly, a new therapeutic approach to Alzheimer’s disease.   

 For information on our recent publications, click on the following link: Rao RV & Buck Institute

Share:
Change text size:
smaller

default

bigger