The Jadiya lab focuses on the role and mechanisms of mitochondrial calcium dysregulation and cell death in aging and age-associated neurodegenerative diseases such as Alzheimer's disease. Mitochondrial calcium flux is an essential regulator of mitochondrial functions and metabolism. However, dysregulated mitochondrial calcium signaling can contribute to oxidative stress, mitochondrial and metabolic derangement, and neuronal cell death. To understand how preserving mitochondrial functions and calcium signaling can prevent neuronal pathology and how these mechanisms could be targeted therapeutically, my lab utilizes genetic, loss, and gain-of-function mutant mice, cutting-edge molecular imaging methodologies, calcium flux analysis, mass spectrometry-based profiling (proteomics, metabolomics, lipidomics), rodent behavioral tests, and cellular metabolism measurements.
- Mitochondrial calcium exchange in Alzheimer's disease. The primary goal of this project is to define how dysregulation in mitochondrial calcium flux affects AD progression.
- Molecular mechanisms of mitochondrial dysfunction and relevance to cellular physiology and disease. My lab aims to investigate the mitochondrial quality control pathways (mitophagy, mitochondrial biogenesis, dynamics, and proteostasis) to determine the mechanisms by which mitochondrial calcium dysregulation and mitochondrial dysfunction contribute to aging and age-related neurodegenerations.
- Brain cell-type-specific mitochondrial calcium signaling and dysfunction. I aim to define if cell-type-specific mitochondrial calcium signaling impacts mitochondrial function, metabolism, and neuronal function in aging and age-related neurodegenerations.