About FDA

Sumit Sarkar, Ph.D.

Research Biologist — Division of Neurotoxicology

Dr. Sumit Sarkar
Sumit Sarkar, Ph.D.

(870) 543-7391
NCTRResearch@fda.hhs.gov  

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 About  |  Publications  |  Lab Member


Background

Dr. Sumit Sarkar received his doctorate in neuropharmacology and neuroscience from Nagpur University in Nagpur, India in 2001 where he acquired a thorough background in neuropharmacology and toxicology. It was there that he performed research that contributed to the mechanistic understanding of neuropeptides, especially opiates, and their interactions with gonadotropin-releasing hormones in the hypothalamus. Dr. Sarkar studied how neuropeptides serve to affect the regulation of gonadotropin hormone release from the pituitary of the teleost, Clarias batrachus or walking catfish. He received further training during his postdoctoral tenure in Dr. Ronald Lechan’s lab in the Division of Endocrinology and Metabolism at Tufts-New England Medical Center in Boston, Massachusetts in 2000 where he studied “the role of neuropeptides in regulating TRH and CRH in the brain of rodents during fasting and bacterial infection.”

His postdoctoral research helped him confirm that phosphorylation of CREB is an essential step in activating thyroid and stress hormones in the brain, especially in the hypothalamus. This specific work earned him the 2002 Abbott Laboratory “Thyroid Research Clinical Fellowship Award for Best Poster Presentation” at 84th Annual Meeting of Endocrine Society. Additionally, he investigated satiety and feeding-inducing hormones and their effects on thyroid and stress hormones in the brain. Dr. Sarkar then joined the Pharmacology and Toxicology Department at Indiana University, School of Medicine to study “emotional stress-induced cardiac regulation and fever to explore common hypothalamic origins and brain stem mechanisms” (2004-2006). Afterwards, he worked as a clinical research fellow at the Simon Cancer Research Center in Indianapolis for one year. In 2008, he joined Boston Children’s Hospital, Harvard Medical School as a research scientist to study the “role of Endoplasmic Reticulum stress in inducing obesity and diabetes.”

In November 2008, Dr. Sarkar joined the NCTR. Since joining the FDA, Dr. Sarkar has published 30 peer-reviewed publications on which he is the first and corresponding author for eleven and seven, respectively. Dr. Sarkar received an FDA “Special Act Award” for exceptional productivity and special accomplishments as a research scientist and an “Outstanding Service” Group Recognition Award for exemplary work as a member of the NCTR summer student committee. Dr. Sarkar is an adjunct assistant professor in Pharmacology and Toxicology at University of Arkansas for Medical Sciences. He serves as an expert grant reviewer on several scientific committees including the Alzheimer’s Association since 2012. Currently, he is a reviewer for Current Alzheimer Research, Alzheimer’s and Dementia, Neurotoxicology, Journal of Neurochemistry, Molecular Neurobiology, Neurotoxicology and Teratology, Toxicology In vitro, Food Chemical Toxicology, Journal of Toxicology, Journal of Drug and Alcohol Research and a manuscript for Dove Press. In 2018, Dr. Sarkar became a member of the editorial board of Metabolic Brain Disease published by Springer.

Research Interests

Over the last eight years, Dr. Sarkar’s research work has been focused on the effects of various neurotoxicants in the brain vasculature and other components of the neurovascular unit. The components of the neurovascular units (pericytes, microglia, astrocytes, and neurons, as well as basal lamina) act as an intricate network to maintain the neuronal homeostatic microenvironment. Thus, disruptions to this intricate cell network due to neurotoxicant exposure can lead to neuronal malfunction and symptoms characteristic of central nervous system diseases. Dr. Sarkar’s laboratory investigates the role of neurovascular elements, ER stress, and endothelial dysfunction in neurodegenerative disorders with a special emphasis on Parkinson’s and Alzheimer’s disease using rodent models. 

Professional Societies/National and International Groups

Endocrine Society
Member
2001 – Present

Sigma Xi
Member
2009 – Present
2016 – 2018 Secretary and Treasurer, local chapter
2018 President, local chapter

Society for Neuroscience – Arkansas Chapter
Member
2009 – Present
2010 – 2013 Secretary
2014 – 2015 Treasurer

Society for Neuroscience
Member
2004 – Present

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Selected Publications

Decreased Mcl-1 Protein Level in the Striatum of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-Treated Mice. 
Lu E., Sarkar S., Raymick J., Paule M.G., and Gu Q.
Brain Res. 2018 Jan 1,1678: 432-439.

Downregulation of 14-3-3 Proteins in a Kainic Acid-Induced Neurotoxicity Model. 
Smani D., Sarkar S., Raymick J., Kanungo J., Paule M.G., and Gu Q.
Mol Neurobiol. 2018 Jan, 55(1): 122-129.

Brain Endothelial Dysfunction Following Pyrithiamine Induced Thiamine Deficiency in the Rat. 
Sarkar S., Liachenko S., Paule M.G., Bowyer J., and Hanig J.P.
Neurotoxicology. 2016 Dec, 57:298-309.

Vascular-Directed Responses of Microglia Produced by Methamphetamine Exposure:  Indirect Evidence That Microglia are Involved in Vascular Repair? 
Bowyer J.F., Sarkar S., Tranter K.M., Hanig J.P., Miller D.B., and O’Callaghan J.P.
J Neuroinflammation. 2016 Mar; 13(1):64, doi: 10.1186/s12974-016-0526.

Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice.
Sarkar S., Raymick J., Ray B., Lahiri D.K., Paule M.G., and Schmued L.
Curr Alz Res. 2015; 12(9): 837-46.

Histopathological and Electrophysiological Indices of Rotenone-Evoked Dopaminergic Toxicity: Neuroprotective Effects of Acetyl-L-Carnitine.
Sarkar S., Gough B., Raymick J., Beaudoin M.A., Ali S.F., Virmani A., and Binienda Z.K.
Neurosci Lett. 2015 Oct, 606: 53-9.

Chronic MPTP Treatment Produces Hyperactivity in Male Mice Which is not Alleviated by Concurrent Trehalose Treatment.
Ferguson S.A., Law C.D., and Sarkar S.
Behav Brain Res. 2015 Oct, 292: 68-78.

Neuroprotective Effect of the Chemical Chaperone, Trehalose, in a Chronic MPTP-Induced Parkinson's Disease Mouse Model.
Sarkar S., Chigurupati S., Raymick J., Mann D., Bowyer J.F., Schmitt T., Beger R.D., Hanig J.P., Schmued L.C., and Paule M.G.
Neurotoxicology. 2014 Sep, 44: 250-62.

Neurovascular Changes in Acute, Sub-Acute and Chronic Mouse Models of Parkinson's Disease.
Sarkar S., Raymick J., Mann D., Bowyer J.F., Hanig J.P., Schmued L.C., Paule M.G., and Chigurupati S.
Curr Neurovasc Res. 2014 Feb, 11(1): 48-61.

In Situ Demonstration of Fluoro-Turquoise Conjugated Gelatin for Visualizing Brain Vasculature and Endothelial Cells and Their Characterization in Normal and Kainic Acid Exposed Animals.
Sarkar S., Raymick J., Paule M.G., and Schmued L.
J Neurosci Methods. 2013 Oct, 219(2): 276-84.

Characterization of Myelin Pathology in the Hippocampal Complex of a Transgenic Mouse Model of Alzheimer’s Disease.
Schmued L.C., Raymick J., Paule M.G., Dumas M., and Sarkar S.
Curr Alzheimer Res. 2013 Jan, 10(1): 30-7.

In Vivo Administration of Fluorescent Dextrans for the Specific and Sensitive Localization of Brain Vascular Pericytes and Their Characterization in Normal and Neurotoxin Exposed Brains.
Sarkar S., and Schmued L.
Neurotoxicology. 2012 June, 33(3): 436-43.

Temporal Progression of Kainic Acid Induced Changes in Vascular Laminin Expression in Rat Brain with Neuronal and Glial Correlates.
Sarkar S., Raymick J., and Schmued L.
Curr Neurovasc Res. 2012 May, 9(2): 110-9.

Kainic Acid and 3-Nitropropionic Acid Induced Expression of Laminin in Vascular Elements of the Rat Brain.
Sarkar S., and Schmued L.
Brain Res. 2010 Sep, 1352: 239-47.

Stress- and Lipopolysaccharide-Induced C-Fos Expression and Nnos in Hypothalamic Neurons Projecting to Medullary Raphe: A Triple Immunofluorescent Labeling Study.
Sarkar S., Zaretskaia M.V., Zaretsky D.V., Moreno M., and DiMicco J.A.
Eur J Neurosci. 2007 Oct, 26(8): 2228-38.

Central Administration Of Cocaine- and Amphetamine-Regulated Transcript Increases Phosphorylation of CAMP Response Element Binding Protein (CREB) in Corticotropin-Releasing Hormone-Producing Neurons but not in Prothyrotropin-Releasing Hormone-Producing Neurons in the Hypothalamic Paraventricular Nucleus.
Sarkar S., Wittman G., Fekete C., and Lechan R.M.
Brain Res. 2004 Mar, 999(2): 181-92.

Glucagon like Peptide-1 (7-36) Amide (GLP-1) Nerve Terminals Densely Innervate Corticotropin-Releasing Hormone Neurons in the Hypothalamic Paraventricular Nucleus.
Sarkar S., Fekete C., Légrádi G., and Lechan R.M.
Brain Res. 2003 Sep, 985(2): 163-8.

Central Administration of Neuropeptide Y Reduces Alpha-Melanocyte-Stimulating Hormone-Induced Cyclic Adenosine 5’-Monophosphate Response Element Binding Protein (CREB) Phosphorylation in Pro-Thyrotropin-Releasing Hormone Neurons and Increases CREB Phosphorylation in Corticotropin-Releasing Hormones Neurons in the Hypothalamic Paraventricular Nucleus.
Sarkar S., and Lechan R.M.
Endocrinology. 2003 Jan, 144(1): 281-91.

Intracerebroventricular Administration of Alpha-Melanocyte Stimulating Hormone Increases Phosphorylation of CREB in TRH- and CRH-Producing Neurons of the Hypothalamic Paraventricular Nucleus.
Sarkar S., Légrádi G., and Lechan R.M.
Brain Res. 2002 Jul, 945(1): 50-9.

Seasonal Changes in Beta-Endorphin-Like Immunoreactivity in the Olfactory System in the Female Catfish, Clarias Batrachus (Linn).
Sarkar S., and Subhedar N.
Gen Comp Endocrinol. 2001 Aug, 123(2): 127-36.

Glucagon-Like Immunoreactivity in the Forebrain and Pituitary of the Teleost, Clarias Batrachus (Linn).
Sarkar S., and Subhedar N.
Gen Comp Endocrinol. 2001 Jan, 121(1): 23-31.

Beta-Endorphin and Gonadotrophin-Releasing Hormone in the Forebrain and Pituitary of the Female Catfish, Clarias Batrachus: Double Immunolabelling Study.
Sarkar S., and Subhedar N.
Gen Comp Endocrinol. 2000 Apr, 118(1): 39-47. 

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Lab Member

James Raymick
Bio Science Laboratory Technician
(870) 543-7391
NCTRResearch@fda.hhs.gov  

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