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These similarities with our model carrying TrKB depletion in iSPNs suggest a new concept for BDNFTrkB signalling in the context of striatal protection modulating dopamine circuits through metabolic pathways such as glutathioneascorbate and energy metabolism
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These damaged cells release harmful inflammatory signals, disrupting the delicate environment needed for healthy brain function
Presented for research literature review only Thompson WG et al
It also maximizes its glutathione content
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