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TBI-induced ischemia, due to reduced CBF or microvascular damage that impedes blood glucose delivery despite preserved CBF, causes increased utilization of all these energy sources, which subsequently stresses cellular glucose/glycogen/lactate stores within the first few hours after injury [39, 59, 60]

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GCLC-KO mice showed activation of C1q, which triggers engulfment of neurons by microglia, and disease-associated-microglia (DAM), suggesting that activation of microglia is linked to the neuronal loss

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1 2 3 4 "Microbial production of vitamin B12: a review and future perspectives"