Sumit Sarkar Ph.D.

Research Biologist — Division of Neurotoxicology

Sumit Sarkar, Ph.D.
(870) 543-7121
NCTRResearch@fda.hhs.gov

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Background

Dr. Sarkar received his doctorate in neuropharmacology and neuroscience from Nagpur University, Nagpur, India in 2001 where he acquired a thorough background and expert skills in neuropharmacology and toxicology. His research contributed to the mechanistic understanding of neuropeptides, especially opiates, and their interactions with gonadotropin releasing hormones in the hypothalamus. In 2000, Dr. Sarkar received further training during a postdoctoral tenure in Dr. Ronald Lechan’s lab in the Division of Endocrinology and Metabolism at Tufts-New England Medical Center, Boston, where he studied the role of neuropeptides in regulating thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH) in the rodent brain during episodes of fasting and bacterial infections. His postdoctoral research confirmed that the phosphorylation of CREB is an essential step in activating thyroid and stress hormones in the brain. This specific work earned him the 2002 Abbott Laboratory “Thyroid Research Clinical Fellowship Award for Best Poster Presentation” at the 84th Annual Meeting of Endocrine Society. Later at Indiana University, Dr. Sarkar studied emotional stress-induced cardiac regulation and fever to explore common hypothalamic origins and brain stem mechanisms, and found a common locus which is the key in thermoregulation, locomotion, and heart rate. Thereafter, he worked as a clinical research fellow in the Simon Cancer Research Center in Indianapolis for one year and in 2008, he joined Boston Children’s Hospital, Harvard Medical School, as a research scientist to study the role of ER stress in inducing obesity and diabetes.

In November 2008, Dr. Sarkar joined NCTR and has since published 57 peer-reviewed publications on which he is the first and corresponding author for twenty-two and twelve, 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 in the Department of Neurobiology at University of Arkansas for Medical Sciences. Dr. Sarkar serves as an expert grant reviewer on several scientific committees including Alzheimer’s Association since 2012. Currently Dr. Sarkar 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 manuscript for Dove Press. In 2018, Dr. Sarkar became a member of the editorial board of the journal, Metabolic Brain Disease, published by Springer and Current Alzheimer’s Research by Bentham Publishers.

Research Interests

Over the last twelve 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. As the Division of Neurotoxicology’s expert on Alzheimer’s disease (AD), Dr. Sarkar has established collaborative studies with others. More recently, Dr. Sarkar’s laboratory has focused on two important areas of Alzheimer’s disease: 1) investigating the role of microvasculature and diet in altering neuropathology in rodent models of AD and 2) comparative intestinal and neuronal pathology for biomarker identification and its correlation with the microbiome in Alzheimer’s disease using AD Tg rats and postmortem tissues.

Professional Societies/National and International Groups

Endocrine Society
Member
2001 – Present

Sigma Xi
Member
2009 – Present

Secretary and Treasurer, local chapter
2016 – 2018

President, local chapter
2018 President

Society for Neuroscience – Arkansas Chapter
Member
2009 – Present

Secretary
2010 – 2013

Treasurer
2014 – 2015

Society for Neuroscience
Member
2004 – Present

Selected Publications

Impaired Aβ Clearance Leads to Vascular Dysfunction in a Transgenic Mice Model of Alzheimer’s Disease.
Rosas-Hernandez H., Cuevas E., Raymick J., Robinson B., and Sarkar S.
Neuroscience. 2020, 440: 48-55.

Characterization of Serum Exosomes from a Transgenic Mouse Model of Alzheimer's Disease.
Rosas-Hernandez H., Cuevas E., Raymick J.B., Robinson B.L., Ali S.F., Hanig J., and Sarkar S.
Curr Alzheimer Res. 2019, 16(5):388-395; PMID:30907317.

Increased Inflammation in BA21 Brain Tissue from African Americans with Alzheimer’s Disease.
Ferguson S.A., Varma V., Sloper D., Panos J.J., and Sarkar S.
Metab Brain Dis. 2020, 35(1):121-133; PMID: 31823110.

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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 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, 945(1): 50-9.