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Immune cells-particularly CD8+ T cells-are highly dependent on mitochondrial ATP supply, and this bioenergetic failure limits their proliferation, cytokine production, and cytotoxic activity, contributing to T cell exhaustion ( As noted earlier, damaged or released mtDNA activates innate immune pathways such as cGAS-STING and NLRP3, sustaining chronic inflammation and inflammaging ( Thus, mtDNA is both a target of HIV-induced damage and a central mediator of downstream immunometabolic dysfunction

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In other overexpression models, -synuclein does not result in robust neuronal death, which may be a function of the cell type expressing this protein and the amount of -synuclein expressed per cell (e.g., the formation of toxic oligomers) (Matsuoka et al