Photo of Rajkumar  Verma, Ph.D.

Rajkumar Verma, Ph.D.

Assistant Professor
Academic Office Location:
Neuroscience
UConn Health
263 Farmington Avenue
Farmington, CT 06030
Phone: 860-679-4552
Email: raverma@uchc.edu
Website(s):

Neuroscience Graduate Program

Dr. Verma is an assistant professor in the Department of Neuroscience and the Pat and Jim Calhoun Cardiology Center at the UConn Health in Farmington, CT since 2016. Rajkumar completed his Ph.D. work at Central Drug Research Institute, Lucknow, India and earned his doctoral degree in pharmacy/pharmacology from Birla Institute of Technology, Mesra, Ranchi, India.

Education
DegreeInstitutionMajor
B.PharmHNB Garhwal UniversityPharmaceutical Sciences
M.PharmBirla Institute of TechnologyPharmacology
Ph.D.Birla Institute of TechnologyPharmacology

Awards
Name of Award/HonorAwarding Organization
First prize winner of the 2018 Stroke Progress and Innovation award by American Heart Association (AHA)American Heart Association
START PPOC awardOffice of Vice President for Research, University of Connecticut
Career development awardAmerican Heart Association
Atomwise Artificial Intelligence Molecular Screen (AIMS) awardAtomwise Inc San Francisco, CA 94105
Travel award, ISN Advanced School 2015, Fitzroy Island, AustraliaInternational Society for Neurochemistry
Junior Investigators Travel Award, International stroke conference, 2015American Heart Association
Outstanding presentation award, Neurosciences retreatDept of Neurosciences, UConn Health
Postdoctoral training grantAmerican Heart Association
Tokuji Ikenaka Prize ‘Gold Award’ for best poster presentation in 10th biennial meeting of Asia Pacific Society for Neurochemistry (APSN) Phuket, ThailandInternational Society for Neurochemistry/ APSN chapter

CNS and CVS Pharmacology to Pharm D students. Neurobiology of Disease

My lab investigates the cause-effect-relationships of stroke outcome. we focus on following three specific areas of stroke research.


Project 1: Stroke remains a leading cause of disability in the United States. Despite recent advances, interventions to reduce damage and enhance recovery after stroke are absent. In this project we will investigate a novel drug target “Purinergic receptor P2X4” for therapeutic exploitation in stroke. We will determine how the inhibition of P2X4R signaling influences these excessive immune during stroke using mice genetically engineered for global or selective deletion of P2X4R in total myeloid or infiltrating myeloid population and also by using pharmacological modulation. The overall goal of this project is to determine if modulation of P2X4R signaling in myeloid cells is a viable therapy for stroke, working towards our long-term goal of developing and identifying target-based therapies for stroke.


Project 2: Vascular dementia (VaD) is the second most common form of dementia after Alzheimer’s disease (AD). Although it is the most rapidly increasing disorder in the aging population, VaD remains under diagnosed, studied and treated. Among many potential clinical triggers, multi-embolic infarcts and cerebral hypoperfusion are major causes of VaD. Among many subtypes of VaD, multi-infarct dementia is the most prominent one which results from multiple lesion or infarcts in brain parenchyma. At the molecular level, VaD is characterized by key neuronal and dendro-synaptic changes resulting in dysfunction and cognitive deficits. Therefore, greater understanding of the pathophysiology at the molecular level is needed to identify novel vascular substrates of dementia. Our goal here is to identify key proteins involved in modification of brain pathology during progression of VaD.


Project 3: MicroRNAs (miRNAs) are short non-coding RNAs and have emerged as a powerful intervention tool for many diseases including stroke. They regulate a broad spectrum of biological pathways through fine-tuning of protein expression levels and altering gene expression levels. miRNA can concurrently target multiple effectors of pathways involved in stroke pathology. In this project we focus on the differential expression of miRNA expressed in mice after stroke and determine if blocking (with genetic deletion or antagomirs) or enhancing (mimics) these target miRNA modulates their effects. The overall goal our lab is to determine if manipulation of target miRNAs can improve functional recovery after stroke

Accepting Lab Rotation Students: Summer '19, Fall '19, Spring '20

Journal Articles

Notes

  • Pubmed article link:
    http://www.ncbi.nlm.nih.gov/myncbi/1pMGjK8l8VkA5/bibliography/47933112/public/?sort=date&direction=ascending

Reviews

  • Synaptopathies: synaptic dysfunction in neurological disorders.
    Lepeta, Katarzyna; Lourenco, Mychael V; Schweitzer, Barbara C; Martino Adami, Pamela V; Banerjee, Priyanjalee; Catuara-Solarz, Silvina; de La Fuente Revenga, Mario; Guillem, Alain Marc; Haidar, Mouna; Ijomone, Omamuyovwi M; Nadorp, Bettina; Qi, Lin; Perera, Nirma D; Refsgaard, Louise K; Reid, Kimberley M; Sabbar, Mariam; Sahoo, Arghyadip; Schafer, Natascha; Sheean, Rebecca K; Suska, Anna; Verma, Rajkumar; Vicidomini, Cinzia; Wright, Dean; Zhang, Xing-Ding; Seidenbecher, Constanze Journal of neurochemistry 2016 Jun;138785-805