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Simplistically, mitochondrial trafficking is subject to pernicious cause or consequence cycles, such as (1) reduced energy from mitochondrial dysfunction causing disorganisation of microtubule networks and α-synuclein protein aggregation, or (2) α-synuclein deposition impairing mitochondrial dynamics and axonal trafficking leading to chaotic organellar distribution, synaptic accumulation of autophagosomes and mitochondrial dysfunction (Esteves et al., 2014

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Moreover, in methionine–choline deficiency-induced fatty liver disease, betaine promotes cytoprotective Akt/mTOR signaling and modifies the autophagy process

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