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The LRRK2 mutations impair synaptic vesicle endocytosis, leading to alterations of DA metabolism and DA-mediated toxic effects in dopaminergic neurons derived from iPSCs generated from reprogrammed PD patient fibroblasts carrying LRRK2 mutations [132]

The glucagon receptor component does not appear to cause significant glucose-raising effects in the context of GLP-1 co-activation, suggesting that the three receptor pathways balance each other in important ways

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A blocked methylation cycle can also become a detoxification problem