NIH R01 · 2024
Synaptic defects caused by mitochondrial complex I dysfunction
PROJECT SUMMARY Background and Objectives: Neurons and their synapses require high amounts of energy to sustain normal levels of activity. Mitochondria are the main energy source, producing ATP via oxidative phosphorylation. In turn, oxidative phosphorylation proceeds through the action of large protein complexes, like Mitochondrial Complex I (MCI). But much work shows that mitochondrial components in neurons and at synapses also do far more than generate ATP. Mitochondria buffer calcium, drive Reactive Oxygen Species (ROS) signaling, and influence cell survival. Using the Drosophila melanogaster neuromuscular junction (NMJ) as a model synapse, we found loss of MCI components impact…
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