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Jaruskova M, et al

Additionally, inhibition of CD38 in the AD mouse model restored NAD + levels, decreased mitochondrial ROS production and plaque depositions in the hippocampus and cortex, and improved cognitive abilities 158

Int J Dev Biol 56(1012):809817 Chen Y, Jungsuwadee P, Vore M, Butterfield DA, St Clair DK (2007) Collateral damage in cancer chemotherapy: oxidative stress in nontargeted tissues

Another study reported that a humanmouse monoclonal antibody binding to methylphenidate, named anti-METH antibody (mAB7F9), elicited a significant reduction in the METH concentration ( Drugs for Chronic Damage Long-term exposure to METH leads to DA depletion, impairment of dopaminergic markers, and neuronal degeneration ( cis -retinoic acid (9cRA), a biologically active derivative of Vit.A, reversed the METH-induced decrease in immunoreactivity and apoptosis of T-helper cells via inhibition of the export of nuclear receptor 77 from the nucleus to the cytosol in primary cultured dopaminergic neurons

As described earlier, the redox control of these signalling pathways can occur at several signalling intermediates