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Dr. Abhik Sen
Scientist D
Date of Birth: 27-07-1978
Sex: Male Male
Date of Joining in ICMR: 03.06. 2019
Designation: Scientist D
Discipline: Molecular Biology
Date of Joining in Present Post: 03.06.2019
Office: ICMR- Rajendra Memorial Research Institute of Medical Sciences, Department of Health Research,
Ministry of Health & Family Welfare,
Government of India, Agamkuan, Patna-800007
Telephone: 0612- 2631565
Fax: 0612-2634379
Residence: RMRIMS Campus (ICMR) Agamkuan, Patna-800007
Mobile: 09875657367
E-Mail: abhik.sen@icmr.gov.in, abhiksen78@gmail.com
Educational Qualifications:
  • Ph.D. (2009): University of Calcutta
  • M.Sc. (2002): University of Calcutta.
  • B.Sc. (2000): University of Calcutta.
Research Experience:
Ph.D. Fellow University of Calcutta (ICMR_NICED, Kolkata & ICMR-RMRIMS, Patna) 03.02.2003 - 06.10.2009
Postdoctoral Fellow Blanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA 20.10.2009 – 13.05.2013
Assistant Professor (Research)

Blanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA

14.05.2013 -19.07.2018
Assistant Professor (Research) George & Anne Ryan Institute for Neuroscience, University of Rhode Island
Kingston, Rhode Island, USA
23.07.2018- 15.05.2019
Scientist D ICMR - Rajendra Memorial Research Institute of Medical Sciences, Patna. 03-06-2019 - till date.
  • The Zoological Society, Kolkata
  • Society for Neuroscience.
  • Qualified in GATE (Graduate Aptitude Test in Engineering) 2002.
  • Qualified CSIR-UGC LS National Eligibility Test June-2002, December-2002 and June-2003

Foreign Visits:
  • A.Sen, Md.A.Akbar, N.S.Chatterjee, P.Sen, A.Debnath and P.Das. “Survival of Entamoebahistolytica in high oxygen environment: A molecular biological study.” at the “3rd Global Meet on Parasitic Diseases” on January 12 – 16, held at Bangalore, India. (2004)
  • A.Sen, Md.A.Akbar, N.S.Chatterjee, N.Nandi, and P.Das. “Survival strategies of Entamoebahistolytica in high oxygen environment”. at “EMBO-Workshop on Pathogenesis of Amoebiasis-From Genomics to Diseases” on November 17th and 18th, held at EinGedi, Israel.(2004)

  • A.Sen, and P. Das “Studies on the role of 29kDa protein of Entamoebahistolytica in survival of the parasite during oxidative stress”. Oral presentation at the “93rd India Science Congress” from 3rd to 7th January 2006 at Hyderabad, India.

  • A.Sen, N.S.Chatterjee, Md.A.Akbar, N.Nandi, and P.Das.“Is 29kDa thiol dependent peroxidase responsible for survival of Entamoebahistolytica during oxidative stress?” at the National Symposium on Recent Advavancement on Parasitology Research, organized by Dept of Zoology, University of Calcutta, from 25th to 26th March, 2006.

  • A.Sen, R. Banerjee, N. Nandi and P. Das. “Studies on differentially expressed genes in promastigotes, lesion-derived amastigotes and axenic amastigotes in Leishmaniadonovaniusing genomic DNA microarray technique.” Oral presentation in the 18thNational Parasitology Congress, IICB, Kolkata from 22nd Nov – 24th Nov, 2006.

  • A.Sen and P.Das. “Whether survival of Entamoebahistolytica is dependent on thiol peroxidase in high oxygen environment” at 20th National Congress of Parasitology on November 3-5, 2008 at NEHU, Shillong.

  • A.Sen, R. Banerjee, N. Nandi, S. Kumar, S.Das, A. Kumar, D. Singh and P. Das. “ Differential genes expression in Leishmaniadonovaniamastigotes isolated from three different physiological conditions: some functional studies on Amastin” at Worldleish 4 held at Lucknow from 3rd to 7th February, 2009.

  • A.Sen, D.L.Alkon, T.J. Nelson.PKCε mediated neuroprotection against high molecular weight Aβ1-42 aggregates” at Neuroscience Retreat held at Morgantown 6-7th June 2011.

  • A.Sen, D.L.Alkon, T.J. Nelson.PKCε mediated neuroprotection against high molecular weight Aβ1-42 aggregates” at Neuroscience 2011 held at Washington DC 12-16th November 2011.

  • A.Sen, D.L.Alkon.ApoE dependent epigenetic regulation in brain: ApoE3 exports and ApoE4 imports HDAC4 and 6 to the nucleus. at Neuroscience 2014 held at Washington DC 15-20th November 2014

  • A.Sen, T.J. Nelson. ApoE isoforms differentially regulates cleavage and secretion of BDNF. Neuroscience 2017 held at Washington DC 11-15th November 2017.

  • J. Hongpaisan,A.Sen, T.J. Nelson, D.L. Alkon.Interaction of Aβ, oxidative stress, and PKCεin hippocampal neurons and microvascular endothelium in Alzheimer's disease. Neuroscience 2017 held at Washington DC 11-15th November 2017.

  • Attended Neuroscience 2017 held at San Diego, CA, USA on3-7th November 2018.

  • Attended training on “Detection of Soil Transmitted Helminths using Kato-Katz method” held at ICMR-RMRIMS from 9th July to 14th July, 2019.

  • Attended training on “National Ethical Guidelines for Biomedical Research Involving Human Participants” (ICMR Guidelines), ScheduleY, Good Clinical Practises (GCP) and “Standard Operating Procedures of Ethics Committee” (SOP) held at ICMR-RMRIMS on 16th July, 2019.

  • Attended training on “Learning Ethics, Accountability and Principles in Clinical Research” held at ICMR-RMRIMS, AgamKuan Patna on 5th and 6th September 2019 organized by DNDi.

  • Attended a DST sponsored workshop on “Basic and advanced proteomics techniques” and “OMICS Technologies for Life Sciences” held at IIT – Bombay from 23rd September to 4th October, 2019.
Major achievements:
  • Discovery of an Entamoebahistolytica defense factors responsible for its survival during host tissue invasion. It was demonstrated that knocking down the 29-kDa surface antigen (thiol-dependent peroxidase; Eh29) of Entamoebahistolytica increases its susceptibility to oxidative stress and thus survival against the host defense mechanism.

  • Identification of pathogenic factors regulating host-pathogen interaction in visceral leishmaniasis using 10000 clone DNA microarray.This study identified that in the lesion derived amastigotes nearly 20% more genes are upregulated compared to macrophage derived cases, thus leading to the conclusion that amastigotes in in-vivo condition in the presence of host immune and signaling defense express different genes than when they infect macrophages in in-vitro conditions.

  • Role of Protein kinase C epsilon (PKCε) in synaptogenesis and Alzheimer’s disease. Our findings concluded that deficits of PKCε function could contribute to the synapse loss in AD, while the therapeutic elimination of such deficits may offer a strategy for the treatment of AD and other synaptic disorders.

  • Discovery of a link between Apolipoprotein E (ApoE), protein kinase C epsilon (PKCε) and epigenetic regulation of brain derived neurotrophic factor (BDNF) in Alzheimer’s disease.This study expands the understanding of the mechanism by which ApoE4 influences epigenetic modifications of gene expression leading to synaptic loss, which is the hallmark of Alzheimer’s disease

  • Role of oxidative stress in Alzheimer’s disease pathology.A reciprocal interaction was demonstrated among oxidative stress, Aβ, and PKCε levels and subsequent PKCε-dependent MnSOD and BDNF expression in hippocampal pyramidal neurons.