During my Postdoctoral studies with Dr. Alan Faden and Dr. David J Loane at the University of Maryland, Baltimore, USA, my primary project was focussed on elucidating the molecular mechanisms of anti-inflammatory microglia activation during traumatic brain injury. We demonstrated that by enhancing the Akt/GSK-3β/CREB signalling, microglia are skewed towards the anti-inflammatory or neuroprotective activation state resulting in the better outcome following traumatic brain injury. These findings recently have been published and selected as the Issue cover of the Journal of Neurochemistry (https://onlinelibrary.wiley.com/toc/14714159/2021/156/2).

During my doctoral studies in Dr Hanif’s laboratory at CSIR-Central Drug Research Institute, India, which is one of the premiere research labs in India, I had the opportunity to work on two interesting projects. The first project involved the understanding the role of glia (astrocytes and microglia) in influencing neuroinflammation and neurogenesis in brain regions associated with memory functions during hypertensive state. The second project was in collaboration with Dr. Rakesh Shukla, (Former Chief Scientist and Head, Pharmacology Department, CSIR-Central Drug Research Institute), where we explored the impact of hypertension and involvement of RAS in chronic neuroinflammation induced neurodegeneration and memory impairment. The findings of these projects have been published in various peer reviewed journals like Brain Behaviour Immunity, Molecular Neurobiology, ACS Chemical Neurosciences etc.

Currently, my lab is interested in studying the role of glia (microglia and astrocytes) in the regulation of neuronal activities in health and disease. More specifically, I am interested in studying the molecular mechanism underlying glia-neuron crosstalk/communication in normal and diseased brain (AD-like pathology). Further, I am also interested in neuropharmacology, neurotoxicology and neurochemistry to screen/identify various bioactive molecules in modulating glia-mediated neurodegeneration, particularly the neuroinflammation, oxidative stress, dysfunctional mitochondria and phagocytosis in the neurodegenerative diseases.