Nilkantha Sen, PhD

Associate Professor

Nilkantha Sen




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, USA

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
Post-Doc Fellowship, 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

An impairment of memory function is one of the major outcomes following TBI. However, the mechanism has not been elucidated yet. In recent efforts, Dr. Sen has found that an induction of ER stress results in an inactivation of a transcription factor CREB and downregulation of a post-synaptic protein, PSD95 which ultimately leads to the cognitive dysfunction. These findings were recently published in the prestigious Journal of Neuroscience. Along with working in the field of studying memory functions following TBI, Dr. Sen has also been studying the effect of alteration in mitochondrial dynamics on synaptic functions following TBI.

One of Dr. Sen’s major strengths is to study the influence of gaseous neurotransmitter on structural and functional alteration of neurons following TBI. Ongoing projects related to studying the role of hydrogen sulfide in the impairment of memory have been published in Molecular Cell.

Vision impairment following TBI is also considered one of the most prominent outcomes and thousands of TBI survivors are suffering from vision related issues. Dr. Sen has shown a compelling evidence in support of the fact that TBI leads to a loss of retinal ganglion cells which are known to connect retina with the visual cortex. Dr. Sen has been continuing studies in this field and elucidating the molecular mechanism responsible for the loss of RGC following TBI.