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Matrix metalloproteinase-9 activation in hyperhomocysteinemic rats is triggered by the opening of the mitochondrial permeability transition pore and antagonism of the N-methyl-D-aspartate receptor-1 (NMDA-R1), resulting in myocyte dysfunction due to elevated calcium overload and oxidative stress [40]

Vagotomy in animal studies is said to disrupt the transfer of -synuclein derived from the gut to the CNS, but human observational evidence is inconsistent, with some studies indicating no change in PD incidence and others suggesting a reduced risk following truncal vagotomy (Elfil et al., 2020)

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