Dr. Shahnawaz Ali Bhat



    Assistant Professor


    Neuroinflammation, Neurodegeneration and Dementia






    Time Table


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 (

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.

  1. Key Publications
    1. Bhat S A, Fatima Z, Sood A, Shukla R, Hanif K. 2021. The Protective Effects of AT2R Agonist, CGP42112A, Against Angiotensin II-Induced Oxidative Stress and Inflammatory Response in Astrocytes: Role of AT2R/PP2A/NF?B/ROS Signaling. Neurotox Res (2021).
    2. Bhat S A., Henry R J., Blanchard A C., Stoica B A., Loane D J. and Faden A I. 2020. Enhanced Akt/GSK?3?/CREB signaling mediates the anti?inflammatory actions of mGluR5 positive allosteric modulators in microglia and following traumatic brain injury in male mice. Journal of Neurochemistry

    3. Bhat, S.A., Goel, R., Shukla, S., Shukla, R., and Hanif, K. 2017. Angiotensin receptor blockade by inhibiting gliosis promotes hippocampal neurogenesis via activation of Wnt/?-catenin signaling in hypertension. Mol Neurobiol. 2018 Jun;55(6):5282-5298. doi: 10.1007/s12035- 017-0754-5. Epub 2017 Sep 7.

    4. Bhat, S.A., Goel, R., Shukla, R., and Hanif, K. 2016. Platelet CD40L induces activation of astrocytes and microglia in hypertension. Brain Behav Immun. 2017 Jan;59:173-189. doi: 10.1016/j.bbi.2016.09.021. Epub 2016 Sep 19.

    5. Bhat, S.A., Goel, R., Shukla, R., and Hanif, K. 2015. Angiotensin receptor blockade modulates NF?B and STAT3 signalling and inhibits glial activation and neuroinflammation better than Angiotensin Converting Enzyme inhibition. Molecular Neurobiology. December 2016, Volume 53, Issue 10, pp 6950–6967.

    6. Bhat, S.A., Sood, A., Shukla, R., and Hanif, K. AT2R activation prevents microglia M1 polarization in a NOX dependent manner: Suppression of ROS-mediated mitochondrial dysfunction and GSK-3?/NRF2 activation in microglia. Molecular Neurobiology.

    7. Goel, R., Bhat, S.A., Hanif, K., Nath, C., and Shukla, R. 2017. Angiotensin II receptor blockers attenuate lipopolysaccharide induced memory impairment by modulation of NF?B mediated BDNF/CREB expression and apoptosis in spontaneously hypertensive rats. Molecular Neurobiology (DOI: 10.1007/s12035-017-0450-5).