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TLR4 gene ablation in a transgenic mouse model of MSA with oligodendroglial -syn overexpression impaired the phagocytic ability of microglia to -syn, leading to enhanced motor impairment and augmented loss of nigrostriatal dopaminergic neurons

Such advances could reopen the therapeutic exploration of controlled mitochondrial uncoupling for metabolic diseases while establishing clearer principles for balancing efficacy and safety

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