About
My journey into the intricate world of neuroscience began in Ph.D, where I explored how early life immune activation (viral mimic, Poly I:C) on the development and aging of the rat brain. I revealed how early immune challenge could induce long-lasting neuroinflammation, impact glial cells, neurotransmitter systems, and eventually affect cognitive and behavioral functions. This work explored important insights into the developmental trajectory of brain plasticity and promoted my interest in molecular mechanisms involved in neuroinflammatory processes. In my doctoral research, I examined how early immune challenges induced changes in the functions and numbers of glial cells and how these changes affected, in turn, spatial memory, fear-conditioned learning, and motor activities. This study utilized various techniques, including intraperitoneal injections, brain perfusion, immunohistochemistry, and biochemical techniques, to profile inflammatory markers and memory-linked genes within the rat brain. My work further extended to behavioral and cognitive-related paradigms, including the Morris water maze and elevated plus maze, giving an entirely rounded view of how early-life immune challenges impact brain function and behavior. Additionally, during my Ph.D. research work, I have developed my proficiency in bioinformatics, including molecular docking and ADMET property prediction for bio-natural and synthetic drugs, which complements my experimental skills, and provides a holistic view of disease mechanisms and treatment possibilities. Next, I pursued postdoctoral training under Professor Cynthia Lemere at the Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, and Harvard Medical School. My postdoctoral work focuses on neuroinflammation in Alzheimer's disease, particularly exploring the role of Complement C3 in mitigating neuroinflammatory responses and protecting cognitive function. My current research involves understanding the influence of C3 protein on Alzheimer's pathology and seeking new potential therapeutic approaches to alleviate AD disease. By utilizing a complement C3 inducible conditional knockout model crossed with APPNL-G-F/NL-G-F knockin mice, I demonstrated that global C3 reduction in adult mice significantly improved cognition and synaptic health despite an unchanged amyloid load. I am now using a tau mouse model (PS30S) to study complement C3 function in tau pathology mice. This ranges from mouse breeding and genotyping to tissue harvest, immunostaining, and confocal imaging, some of which are biochemical techniques. On the molecular side, it extends to qRT-PCR and RNA sequencing to dissect the intricate molecular mechanisms involved. I also performed behavioral testing, including the Open Field, Y-Maze, Rota-rod, and Contextual fear conditioning test, to assess cognitive and behavioral outcomes associated with Complement C3 modulation. My academic and research trajectory, from investigating early-life immune activation to exploring the molecular intricacies of Alzheimer's disease, reflects a deep commitment toward the understanding and addressing of neurodegenerative disorders. Equipped with this background in experimental and computational techniques, I can therefore make very fundamental contributions in neurodegenerative studies. It is my hope to take advantage of the opportunity further to bridge basic neuroscience with translational medicine, aiming to develop such innovative strategies that will, in the end, free patients and society from burdens like those of Alzheimer's disease
Employment
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Brigham and Women's Hospital Postdoctoral Research Fellow2022 - Present
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Jiwaji University DBT-SRF2015 - 2018
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Jiwaji University DBT-JRF2013 - 2015
Education
Education history is unavailable.
Projects & Funding
Projects & funding information is unavailable.
Publications (9)
- C3 lowering in adult APP KI mice rescues synapses and spares cognitive decline Save
- Global C3 lowering in adulthood protects against hippocampal dysfunction and cognitive impairment in aged mice Save
- The complement cascade in Alzheimer’s disease: modern implications of an ancient immune protagonist Save
- Molecular Docking Studies of Bioactive Constituents of Long Pepper, Ginger, Clove, and Black Pepper to Target the Human Cathepsin L Protease: As a Natural Therapeutic Strategy Against SARS-Cov-2 Save
- Early life exposure to poly I:C impairs striatal DA-D2 receptor binding, myelination and associated behavioural abilities in rats Save
- Molecular Docking Based Analysis to Elucidate the DNA Topoisomerase IIβ as the Potential Target for the Ganoderic Acid; A Natural Therapeutic Agent in Cancer Therapy Save
- Poly (I:C) Exposure in Early Life Alters Methylation of DNA and Acetylation of Histone at Synaptic Plasticity Gene Promoter in Developing Rat Brain Leading to Memory Impairment Save
- Targeting Fatty Acid Synthase Protein by Molecular Docking Studies of Naturally Occurring Ganoderic Acid Analogues acting as Anti-Obesity Molecule Save
- Postnatal exposure to poly (I:C) impairs learning and memory through changes in synaptic plasticity gene expression in developing rat brain Save