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Furthermore, exendin-4 administration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in vivo animal model of PD has been shown to inhibit microglial activation thereby minimizing the loss of dopaminergic neurons in the pars compacta of the substantia nigra and the striatum [78]

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GSH augmentation deserves investigation as a beneficial therapeutic approach for not only PD but also numerous other CNS disorders for which GSH deficiency and GSH-related enzyme deficits have been documented (multiple sclerosis, 25,26 autism, 2729 Alzheimers disease, 30,31 schizophrenia, 32,33 and bipolar disease 34 )