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In addition, genetic glutathione synthetase defects (Figure 2, reaction 5), also an autosomal recessive trait, reduce glutathione levels and generate overproduction of 5-oxoproline

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When cardiolipin becomes oxidized, it migrates to the outer membrane, where it can interact with cytoplasmic amyloidogenic proteins to facilitate the formation of pores in the mitochondrial membrane, and, ultimately, to trap mitochondrial debris from aged mitochondria within fibrillar extracellular deposits such as Lewy bodies (Seneff et al., 2025b)