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In another rodent experiment, synthetic TB4 was administered to models of autoimmune encephalomyelitis, markedly decreasing the number of inflammatory cells in the brains of the treated animals [39]

An increasing body of preclinical and clinical evidence suggests that mitochondrial dysfunction, characterized by bioenergetic failure, heightened oxidative stress, dysregulated calcium handling, and impaired mitophagy, contributes to the etiopathogenesis of both CVDs and cognitive impairment

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