Research interests: Parkinson's disease, synaptic endocytic dysfunction, mechanisms for GBA-mediated cognitive dysfunction in Parkinson's disease
1. Synaptic endocytosis dysfunction in pathogenesis of Parkinson’s disease: Synapses are the functional sites through which neurons communicate and their dysfunction is increasingly implicated in neurodegenerative disorders including Parkinson’s disease (PD). Pre-synaptic proteostasis dysfunction in striatum is considered as key early event in PD pathogenesis, though the mechanisms are still elusive. Chaperones in the synapse play an important role in synaptic proteostasis by preventing protein misfolding and aggregation. They mainly consist of heat shock protein 40s (Hsp40 or DNAJs) forming localized complexes with Hsc70. The DNAJC6 or Auxilin is one such co-chaperone that plays a central role in uncoating clathrin coated vesicles to facilitate smooth synaptic vesicle endocytosis. Its mutation has been implicated in juvenile/early onset PD. In this study, we intend to understand the molecular mechanisms by which loss of auxilin causes PD via characterization of auxilin knockout (KO) mice and also by using induced pluripotent stem cell (iPSC) derived and primary neuronal cultures.
2. Mechanisms for GBA-mediated cognitive dysfunction in PD: Mutations in GBA that encodes glucocerebrosidase 1 which lead to accumulation of glycosphingolipids, is the most common genetic risk factor for PD. Cognitive dysfunction is more prevalent and severe in PD patients with GBA mutations. Here, we propose to use our well-established mouse model of GBA mutations with PD phenotype (Gba/SNCA) to decipher the mechanisms for cognitive decline in PD.
Hobbies: Trekking, biking
Education & Training
- PhDNational Institute of Mental Health and Neurosciences (NIMHANS), Neurophysiology, Parkinson's disease (2018)
- MScKasturba Medical College, Manipal Academy of Higher Education, Medical Physiology (2011)
- BScYuvaraja College, University of Mysore, Biochemistry, Biotechnology & Microbiology (2007)