Veena Prahlad, Ph.D.

Veena Prahlad ,

Associate Professor
Department of Biology

Veena Prahlad, Ph.D., Associate Professor in the Department of Biology, received an undergraduate degree at St. Joseph’s College in Bangalore, India in 1990, a M.Sc. in Life Sciences in 1992 from Jawaharlal Nehru University in New Delhi, India, and a Ph.D. from Northwestern University. She completed two postdoctoral fellowships, one in Genetics at the University of Madison and the other in Molecular Biosciences at Northwestern. 

Cellular protein misfolding leads to the occurrence of amyloid oligomers and protein aggregates and is the cause of cellular dysfunction associated with age-related diseases such as Huntington’s and Alzheimer’s Diseases, cardiomyopthy, adult onset diabetes, cancer and others. All cells possess conserved mechanisms to counteract the toxic effects of protein misfolding. One central mechanism of protection is the heat shock response (HSR) during which activation of the heat shock transcription factor 1 (HSF1) upregulates heat shock proteins (HSPs) to help refold and/or degrade damaged proteins and restore homeostasis. Experimentally eliciting the HSR has resulted in amelioration of disease symptoms in numerous animal models. However, while HSP expression is protective, high levels of HSP expression inhibits basic anabolic activities such as cell growth, division, and secretory function. Thus chaperone levels within cells of a multicellular organism are not maintained in excess but are subject to multiple levels of regulatory control. Therefore, if harnessing the cells cytoprotective mechanisms is to be a viable strategy to intervene in human diseases, one must understand the regulation and co-ordination of such mechanisms at the organismal level.

My laboratory studies how cellular responses to protein damage are regulated within a metazoan.  The major focus of the lab is to understand how inter-tissue signaling mechanisms modulate neuronal health and dysfunction.  We have shown that the HSR in a metazoan is not solely an autonomous response of cells to the damage, but instead under cell non-autonomous control of the nervous system.  We are currently investigating the signaling pathways underlying this control.