The broad area of research includes synaptic homeostasis maintenance by Vitamin D3 in health and diseased conditions. Synaptic impairment underlies a common detrimental effect observed under most neurotoxic conditions, where our research group has shown an antioxidant and neuroprotective property of nutraceutical, Vitamin D3 in a mouse model of HD. We also showed VD administration rescued the expression pattern of key neurotrophic factors in the brain like brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the mouse striatum. We recently provided evidence that the neuroprotective benefits of Vitamin D3 (VD) occurred through a rescue in the protein expression of Vitamin D receptors (VDR).

One of the primary focuses of my laboratory is to decipher the myriad molecular mechanism through which the brain resident immune protein expression like T-cell receptor beta subunit (TCR-β) gets modulated under neuropathological/neurotoxic conditions like Huntington’s disease (HD) or under neuropsychiatric disorders like schizophrenia. People with neurological disorders have psychiatric, cognitive, and motor dysfunction where impairments begin with synaptic pathologies much before the clinical symptoms of the disorder.

Our lab is keen to unravel the different modes of molecular mechanisms undertaken by VD in restoring neuronal functions and synaptic communication in an aged brain and neuropathological condition characterized by increased mitochondrial dysfunction and enhanced oxidative stress. We aim to investigate the downstream molecular pathways responsible for crosstalk between VD and ionotropic receptors at the central nervous system synapses by undertaking in-vivo and in-vitro models. We undertake behavior assays, whole-cell electrophysiology (to monitor neuronal activity), molecular biology, proteomics, and biochemical tools to investigate the myriad outcomes of Vitamin D3 (VD) in the central nervous system.