Sovan Sarkar



Sovan Sarkar (born July 15, 1978) is an Indian scientist working on Autophagy. His graduate and post-doctoral research from University of Cambridge has provided mechanistic insights into the regulation of mTOR-independent autophagy and has led to the discovery of a number of candidate drugs of potential biomedical relevance. He is a post-doctoral associate at the Whitehead Institute for Biomedical Research in Massachusetts Institute of Technology. He is a former Gates Scholar of the Gates Cambridge Scholarship and currently holds the distinction of a Former Fellow at Hughes Hall, a Cambridge University college.

Career
Sarkar went to Calcutta Boys School in Kolkata, India, during which he became fascinated with biology. Following his interest in this subject, he did his undergraduate degree in B.Sc. Physiology from Presidency College, Kolkata, where he secured first rank in University of Calcutta. Thereafter, he studied M.Sc. Biotechnology at the School of Biotechnology in Madurai Kamaraj University where he secured second rank in the university. In 2002, he was awarded the prestigious Gates Cambridge Scholarship established by the Bill and Melinda Gates Foundation for pursuing his doctoral research at the University of Cambridge in UK. He did his Ph.D. at the Department of Medical Genetics in Cambridge Institute for Medical Research (CIMR), University of Cambridge, in the laboratory of David Rubinsztein, during which he was a student at Hughes Hall, a Cambridge University college. From 2006 till 2010, he worked at the University of Cambridge as a Post-doctoral Research Associate in CIMR. In 2007, he was elected as a Research Fellow of Hughes Hall where he is currently a Former Fellow. He is presently working as a Post-doctoral Research Associate at the Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, in the laboratory of Rudolf Jaenisch.

Since Cambridge, Sarkar has been working on Autophagy, which has emerged as a field of rapidly growing interest with implications in various human pathological and physiological conditions. It is cell survival process that also acts an intracellular protein degradation pathway for misfolded and aggregated proteins. His research has provided important mechanistic insights into the regulation of mTOR-independent autophagy and has led to the discovery of a number of candidate drugs of potential biomedical relevance. The vast resource of small molecule autophagy regulators generated from his work has been employed by several research groups not only to study autophagy but also to show beneficial effects in a range of human pathological conditions, including neurodegenerative diseases. These findings have been published in over 30 peer-reviewed international journals, including twice in Nature Chemical Biology, generated a number of patents, and have attracted press releases from the Wellcome Trust UK, including coverages in Nature Reviews Drug Discovery, Cambridge University and Channel 4 news highlighting 'cells could eat brain disorders'. He has received a number of awards with the most notable one being the Biochemical Society Early Career Research Award 2012 in the category of cell biology, which is based on his work on autophagy from the University of Cambridge.

Research
His current research interests include understanding the molecular mechanisms regulating mammalian autophagy and identification of small molecule autophagy enhancers as a therapeutic strategy for neurodegenerative diseases. Autophagy is negatively regulated by the mammalian Target Of Rapamycin (mTOR; a serine/threonine kinase), and can be induced by the mTOR inhibitor rapamycin. However, mTOR has many vital cellular functions like translation and cell growth, and therefore, it is highly desirable to discover mTOR-independent, autophagy-inducing pathways/drugs as therapeutic targets. His work involves in the identification of autophagy modulators that regulate autophagy independently of mTOR. Identification of autophagy-inducing drugs has huge therapeutic potential not only for neurodegenerative diseases, but also for other diseases where autophagy acts as a protective pathway.

The formation of intra-neuronal mutant protein aggregates is a characteristic feature of several human neurodegenerative disorders, like Alzheimer’s disease, Parkinson’s disease, and polyglutamine disorders, including Huntington’s disease and spinocerebellar ataxias. One possible approach to treating such diseases may be to enhance degradation of the mutant proteins associated with neurodegeneration. The autophagy-lysosome and ubiquitin-proteasome pathways are the two major routes for protein clearance in eukaryotic cells. While the ubiquitin proteasome system predominantly degrades short-lived proteins and it is unclear whether it is a feasible therapeutic target, the clearance of aggregate-prone proteins (aggregate precursors) can be achieved by upregulating autophagy that can degrade long-lived proteins, protein complexes and organelles. Autophagy is an intracellular protein degradation pathway for aggregate-prone proteins causing neurodegenerative diseases, such as mutant huntingtin associated with Huntington’s disease, A53T and A30P mutants of alpha-synuclein associated with familial Parkinson's disease, ataxin 3 causing spinocerebellar ataxia type 3, and tau causing fronto-temporal dementias. Autophagic degradation of these mutant proteins correlates with reduced protein aggregation and toxicity, and therefore, enhancing autophagy may be a possible therapeutic strategy for such diseases where the mutant proteins are autophagy substrates.