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Research theme:
My multi-disciplinary group is adopting an integrated approach to drug discovery that combines medicinal chemistry, basic biology, and biochemistry principles for an efficient drug design process. Interests of the group lie in identifying underlying principles in disease pathogenesis to discover new targets, designing molecular intervention strategies, and confirming the biological/therapeutic activities of the designed compounds/formulation. The small molecule/peptide regulators contribute to drug development and the understanding of biological systems in the human body. The pathways and the pathological conditions that we are currently focusing on are:

ER-Stress, Inter-organelle communication and Autophagy

My lab studies mechanisms underlying cellular homeostasis and signalling, focusing on Inter-organelles communication with ER as central and autophagy-lysosome systems. The interest in the ER system in the lab initially emerged through studies to understand how cells respond to different stress conditions. The research group identified ARL6IP5 as a key mediator of ER stress and cellular homeostasis via regulating bulk and selective autophagy via non-canonical pathways and their role in disease pathogenesis.

My lab uses a holistic approach using different genetic and sporadic animal models to understand disease pathogenesis and cellular models for mechanistic insight. Using quantitative proteomics, imaging, and biochemical approaches to elucidate underlying biochemical mechanisms controlling protein turnover, organelles health and applies these approaches to examine regulatory pathways relevant to various neurodegenerative diseases, including Prion, Parkinson's and Alzheimer's. A significant focus currently is the ER-associated proteins, which control the turnover of damaged mitochondria via the autophagy pathway and are differentially regulated in Chronic Disease.

Brain-Bone Axis:

Altered interorgan signalling contributes to inflammation, particularly in neurodegenerative diseases like Alzheimer's (AD). One emerging axis in this context is brain–bone communication, a bidirectional signalling loop increasingly recognized in ageing and AD pathology. Once thought to be passive, Bone actively participates in this process by releasing osteokines and inflammatory mediators from bone marrow immune cells. These factors can cross the blood-brain barrier (BBB) or influence peripheral immune priming, ultimately impacting brain homeostasis. At the same time, the brain sends signals to the Bone. In Alzheimer's and other neurodegenerative diseases, this feedback loop becomes dysregulated leading to impaired bone integrity, immune dysregulation, and exacerbation of brain inflammation. My lab's interest is in understanding this crosstalk to offer novel therapeutic entry points targeting peripheral organs like the bone to protect the ageing brain.

Bone and joint Diseases

Our lab focuses on the molecular and metabolic basis for skeletal formation and bone and cartilage regeneration. We are focusing on regulation of bone remodelling in an age dependent and under chronic inflammatory conditions. The metabolic regulation of osteoblast, osteocytes and osteoclast development and function.

Our foundational research is paving the way for better treatments for skeletal conditions. Our research aims to expand scientific knowledge, ultimately leading to the development of innovative treatments. By uncovering novel insights and validating new therapeutic molecules, we're working toward the rational design of new drugs for osteoarthritis, osteoporosis, and bone cancers.