Fig. 5.

Parkinson's disease.

Above is a figure illustrating mitochondrial affecting pathways in Parkinson's associated with α-synuclein and Parkin. Increased oxidative stress leads to mitochondrial dysfunction, which leads to increased mitochondrial ROS and mitochondrial DNA depletion and deletion. Mitochondrial ROS activate α-synuclein, leading to α-synuclein aggregation in the cytoplasm. These aggregates cause ER dysfunction, synaptic dysfunction, inhibition of ETC complexes 1 and 3, and the formation of Lewy bodies. Lewy bodies cause microglial activation by increasing TNFα, IL1, and IL6, which leads to apoptosis, neuroinflammation, and neuron death. Parkin leads to impaired mitophagy involving both Parkin and PINK1, leading to mitochondrial dysfunction. Parkin also leads to the increase of PGC1, F1GBP, and AIMP2, which leads to neuroinflammation and neuron death.