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On the one hand, in some in vitro or animal models, enhanced BCAA catabolism has been reported to upregulate certain M2-related markers and support alternative activation programs, whereas inhibition of BCAA metabolism may impair the establishment of M2-like phenotypes ( At the molecular level, the coupling of BCAAs with mTORC1 signaling provides a key clue for understanding their pro-inflammatory effects

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10.1039/D5PM00079C 93

ROS accumulation triggers OS, cellular damage, mitochondrial dysfunction, A deposition, Tau hyperphosphorylation, synaptic loss, and neuronal deathkey factors in AD progression (Aliev et al., 2004

Ellinghaus D, Jostins L, Spain SL, Cortes A, Bethune J et al (2016) Analysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared loci