Doctoral Candidate: Sanya Verma

Doctoral Candidate Position 5 - Faculty of Medicine, University of Belgrade, Serbia

Molecular pathways of mitochondria-immune interaction

Sanya completed her Bachelor's degree in Biochemical Engineering and Biotechnology at Indian Institute of Technology Delhi in 2021, which gave her a strong foundation in molecular biology, genetics, enzymology, bioinformatics and bioprocess engineering. Her bachelor's thesis involved building a bioinformatics pipeline for de novo RNA-seq assembly and gene annotation of carbohydrate-active enzymes of a novel bacterium. After completing her bachelor's, she was appointed as Junior Research Fellow at the Department of Biochemical Engineering and Biotechnology at IIT Delhi where she gained a solid research foundation and growing lab independence in fundamental molecular biology methods including bacterial transformation, plasmid isolation, restriction digestion, PCRs and agarose gel electrophoresis.
She then obtained her Master's degree in Biology at the Technical University of Munich in 2025, where she specialised in Medical Biology, Virology and Biochemistry and Cell Biology. During her Master's thesis at Helmholtz Munich, she engineered a novel chimeric endolysin against Gram-positive bacteria, integrating rational protein design, cloning, expression, purification and functional assays. This exposure strengthened her interest in disease biology and in the development of therapeutic concepts.
In parallel, she also explored computational ligand docking through a course and an internship under Prof. Antonella Di Pizio to understand the mechanism of drug modelling i.e., how ligands bind to the receptors in the body and how this interaction drives biological effect. She also undertook internships at Institute of Molecular Immunology, Klinikum Rechts der Isar and at Institute of Virology, Helmholtz Munich driven by her interest in virology and gene therapy strategies. Together, these multidisciplinary experiences broadened her curiosity towards how disease emerges at molecular and cellular levels, and how these mechanisms can be translated into therapeutic opportunities.
Within the BICEPS network, she aims to investigate how mitochondrial dysfunction and AMPK-mediated cellular energy signalling influence immune activation and neuroinflammation in Parkinson's Disease, with the goal of identifying mechanistically informed disease-modifying intervention points within the mitochondria-immune axis.

Description of project

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the brain. Emerging evidence highlights mitochondrial dysfunction as a central factor in PD pathology, with damaged mitochondria contributing to immune activation and neuroinflammation. In this context, disruptions in cellular energy systems, particularly within mitochondria, can trigger harmful responses, including immune system activation. This PhD project aims to uncover the molecular mechanisms by which mitochondrial dysfunction, alongside changes in the activity of the key intracellular energy sensor, AMP-activated protein kinase (AMPK), influences inflammatory responses in PD. By exploring the interplay between cellular energy regulation, oxidative stress, and inflammatory response in PD-related neurodegeneration, we aim to identify potential molecular targets within the AMPK-mitochondria axis that could inform therapeutic strategies for PD-related neurodegeneration.
The research will determine the effects of the most frequent PD-associated mutations (GBA, LRRK2, PRKN and PINK1) on the transcription and protein profiles of mitochondria-inflammatory interaction in genetically altered cell lines and human PBMCs, using omics approaches. The key findings will then be confirmed in skin-derived fibroblasts and iPSCs-derived neurons from patients with most common genetic risks for development of PD, recruited at the Clinic for Neurology, University Clinical Center of Serbia. Finally, using the newly synthesized reactive oxygen species (ROS) inhibitors, their effect on mitochondrial functions will be evaluated.