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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 ( -Synuclein, amyloid- , and huntingtin are other proteins that may follow the same principles for trapping deuterium

Several metabolic intermediates, such as long-chain acylcarnitines can cause oxidative stress at high levels and high levels of ROS can then cause damage to cells and tissues, leading to a further decline in performance

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Deciphering the Molecular Signals of PINK1/Parkin Mitophagy

Ohar, J

Oslund, R