Illuminating the Mitochondria and the Mitochondrial Genome’s role in Neurodegeneration with Nanopipettes
Engineering
Senior Thesis Research in Pourmand Lab (BME 195)
The human brain consumes a lot of energy and oxygen to control all the involuntary, such as heartbeat and metabolism, and voluntary, such as waving your hand, actions of the body. As such, brain cells and neurons are particularly dependent on the role of properly functioning internal organelles called mitochondria. Mitochondria are important subcellular organelles that have a variety of functions. The most notable functions mitochondria serve are to sequester signaling molecules for apoptosis, or cell death, and generate usable energy as adenosine triphosphate (ATP) from oxidative phosphorylation of glucose molecules. This generation of ATP involves a specific balance of free radical reactive oxygen species (ROS), which reacts with DNA and other components of the cell, disrupting regular function. However, like an aging cell, mitochondria also require recycling. Mitochondria house apoptotic factors, which signal cell death. The stress of ROS produced can lead to mitochondria losing function. When too many mitochondria lose function, the mitochondria release the apoptotic factors it sequesters and the neuronal axon shortens. This process leads to the development of neurodegenerative diseases such as Parkinson’s or Alzheimer’s. In this study, we will present our current results of the genomic variance acquired from mitochondria proximal and distal to the main body of neurons in hopes of revealing a mechanism and biomarkers for the onset of energy-deficiency related neurodegenerative diseases.
