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H 2 O 2 produced in higher levels from injured microglia increases ROS production which proceeds to cause oxidative stress and aftermath features like DNA fragmentation, protein oxidation, lipid peroxidation, apoptosis

Failure to promptly repair these damages may lead to genomic instability and abnormal cellular function, and may even drive pathological processes such as cancer, neurodegenerative diseases and autoimmune diseases (1,4-6)

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Butner LE, Fulco PP, Feldman G, et al

One particularly instructive example comes from research using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced models of PD, where chronic administration of monoacylglycerol lipase inhibitors was found to not only preserve dopaminergic neurons in the substantia nigra but also induce a distinctive microglial activation profile characterized by increased release of neurotrophic factors and decreased expression of classical inflammatory markers [459]