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The mitochondrial permeability transition from in vitro artifact to disease target

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The protective effects of low dose carbon monoxide in the -synuclein model are associated with increases in cathepsin D and reduced -synuclein pathology To determine the mechanism by which CO promoted survival of dopaminergic neurons, we next assessed whether CO administration affected cellular mechanisms of protein degradation, including autophagy and lysosomal function, as well as levels of Syn and Syn aggregates, which have been proposed to mediate neuropathology in PD patients 1