Mutations in the ATP13A2 Gene and Parkinsonism: A Preliminary Review
Figure 1
Model of how ATP13A2 expression may affect lysosomes and mitochondria to prevent neurodegeneration. (a) After α-synuclein has been internalized by autophagosomes, it can be immediately degraded in lysosomes containing ATP13A2 or secreted out of the cell via multivesicular bodies (MVBs) also containing ATP13A2. Both routes prevent intracellular accumulation of α-synuclein. (b) Knocking out ATP13A2 expression in neurons leads to mitochondrial defects, resulting in higher intracellular levels of reactive oxygen species (ROS) and Ca2+, both of which contribute to neurodegeneration.
