Parkinson’s disease (PD) is a complex neurodegenerative disorder involving the loss of dopaminergic neurons from substantia nigra region of brain, and the aetiology and molecular mechanisms behind the loss of neurons are not completely understood. But mitochondrial dysfunction is known to be the major factor leading to neuro-degeneration. Moreover, microRNAs have now been considered as essential players in virtually every biological process. Interestingly, the presence of mitochondrially-located miRNAs also suggests its mitochondrial regulation. TRIM family of E3 ubiquitin ligases has been known to regulate inflammatory processes, autophagy and cell death. These proteins are also involved in regulation of mitochondrial function as some of the TRIMs have been known to localize to and associate with mitochondria and regulate its function. Therefore, I am interested in studying the role of a particular NHL domain containing TRIM members (TRIM2, TRIM3, TRIM32 and TRIM71) in regulation of mitochondrial function in PD-condition. These TRIM-NHL proteins are important in neurodevelopment aspect and their mutation can lead to several neuro-developmental disorders. As the NHL domain is known to interact with many mRNAs and miRNAs, it will be interesting to study their role in translocating the miRNAs to mitochondria and regulate the mitochondrial function in PD condition.