Nilkantha Sen, PhD

  • Associate Professor

Nilkantha Sen, PhD, joined the University of Pittsburgh Department of Neurological Surgery in March of 2017 as an associate professor.

After graduating from Indian Institute of Chemical Biology—one of the most prestigious institutes of India—Dr. Sen joined Johns Hopkins University in 2010 as a post-doctoral fellow under the mentorship of Solomon H. Snyder, MD. His work studied the mechanism involved for nitric oxide-induced neuronal cell death and he discovered a novel mechanism which was shown to play a key role in cell death associated with several neurodegenerative diseases such as Alzheimer’s Disease, Parkinson’s Disease and brain injury.

Dr. Sen also identified a novel neuroprotective protein, GOSPEL, which can protect cell death in the brain during neurodegeneration. Furthermore, his findings further clarified the molecular mechanism associated with both hyperactivity and neurotoxicity following exposure of cocaine, providing a new insight in the field of drug abuse.

While working in the field of nitric oxide, Dr. Sen also explored another newly discovered gasotransmitter, hydrogen sulfide (H2S) in the brain and in peripheral tissues such as the liver. However, its role in physiology and pathology was poorly understood. Dr. Sen found that, like nitric oxide, H2S also modifies proteins through a process of sulfhydration and shows that sulfhydration of several proteins affects their biological functions and influences the outcome of neurodegenerative diseases.

In 2012, Dr. Sen joined Georgia Regents University as an assistant professor and started working in the field of traumatic brain injury. His major interest in TBI is to understand the role of gasotransmitter in the pathology. Recently, he has identified a novel mechanism that can explain the edema and cell death following TBI.

Dr. Sen has published 38 papers in refereed journals including seven review articles. Total citations have exceeded 2500.

Specialized Areas of Interest

Elucidating molecular mechanisms associated with pathology of TBI; cognitive dysfunction, memory impairment and vision impairment following TBI; pre-clinical testing of potential compounds against TBI in mice model

Professional Organization Membership

Indian Science Congress Association, India
Society of Biological Chemistry, India
Society for Neuroscience

Education & Training

  • BSc, Chemistry, Calcutta University, India 1998
  • MSc, Biochemistry, Calcutta University, India, 2000
  • PhD, Oxidative Stress, Cell Death, Indian Institute of Chemical Biology, 2006
  • Fellow, Neuroscience, Johns Hopkins Medical College, USA, 2010

Honors & Awards

  • Emerging Scientist Award, Augusta University, Ga., 2016
  • Young Outstanding Basic Science Faculty Award, Georgia Regents University, 2016
  • Oral Podium Award, 2nd International Conference on H2S Biology and Medicine, 2012
  • Young Scientist Award (W. Barry Wood, Jr), Johns Hopkins University, 2010
  • Third Prize, Annual Poster Competition, Johns Hopkins University, 2009
  • Best Poster Award, International Symposium on Molecular Mechanism of Diseases, 2005

Selected Publications

Sen T, Sen N. Isoflurane-induced inactivation of CREB through histone deacetylase 4 is responsible for cognitive impairment in developing brain. Neurobiology of Disease  96:12-21, 2016.

Sen T, Sen N. Treatment with an activator of hypoxia-inducible factor 1, DMOG provides neuroprotection after traumatic brain injury. Neuropharmacology 107:79-88, 2016.

Mir S, Sen T, Sen N. Cytokine-induced GAPDH sulfhydration effects PSD95 degradation and memory. Molecular Cell 56(6):786-95, 2014.

Kapoor S, Farook JM, Saha R, Sen N. Foxo3a Transcriptionally up-regulates AQP4 and induces cerebral edema following Traumatic Brain Injury. Journal of Neuroscience 33(44):17398-403, 2013.

Farook JM, Shields J, Tawfik A, Markand S, Sen T, Smith SB, Brann D, Dhandapani KM, Sen N. GADD34 induces cell death through inactivation of Akt following traumatic brain injury. Cell Death and Disease 4:e754, 2013.

Research Activities

Dr. Sen has been continuing his effort to identify novel therapeutic strategies to attenuate cognitive and visual dysfunction following traumatic brain injury (TBI). Recently his lab identified that a decrease in mitochondrial mass contributes to the mitochondrial dysfunction which is primarily responsible for cognitive dysfunction following TBI. As part of the mechanism, an augmentation in cyclin D1 affects the transcriptional activity of a key factor which critically regulates mitochondrial mass.

In addition, recent studies have shown that TBI is one of the major causes of neurodegenerative diseases such as Alzheimer’s disease, which is characterized by tauopathy. Dr. Sen found that an increase in acetylation of Tau induced by nitric oxide contributes to tauopathy. To elucidate the molecular mechanism, Dr. Sen found that an increase in nitrosylation of a rate-limiting glycolytic enzyme GAPDH facilitates Tau acetylation and tauopathy. Dr. Sen’s lab is in the process of understanding whether Tau acetylation contributes to tauopathy following TBI.