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Helicobacter pylori induced apoptosis

S.et al

The idea is supported by maintenance of functional GSH/GSSG levels by Sp in BSO and neurotoxin treated cells as compared to untreated ones which showed a significant decline in the antioxidant ratio probably, due to enhanced formation of glutathionequinones 43

Future research will focus on decoding metabolic regulationsuch as CSF1R-mediated resting-state energy metabolism and AMPK/mTOR-controlled activated-state metabolic remodelingand targeting BDNF neurotrophic or TNF- pro-inflammatory signaling to develop precision therapies for neurodegenerative diseases, leveraging microglial metabolic-immunological crosstalk (Salter and Stevens, 2017)