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Impaired mitochondrial redox homeostasis, such as oxidative stress due to excessive ROS production and impairment of antioxidant function, can cause mitochondrial dysfunction and the onset of the cell death cascade, leading to neuronal damage (115, 116)

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Within the methionine cycle, 5-methylTHF acts as a co-substrate in the remethylation of homocysteine to methionine via the B 12 -dependent enzyme methionine synthase

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It has been established that intramitochondrial Ca 2+ triggers a cascade of processes within the mitochondrion that increase ATP synthesis through oxidative phosphorylation, the activation of three dehydrogenases in the tricarboxylic acid (TCA) cycle, which facilitates increased generation of NADH and consequently the transfer of electrons to an acceptor such as O 2 (Gunter et al., 2004[178])