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Copper and CuNPs have the ability to stimulate apoptosis by caspase-dependent and independent pathways through induction of pro-apoptotic protein (Bax) and suppression of anti-apoptotic protein (Bcl-2) [66, 90, 96], while chrysin activates apoptosis through intrinsic pathways of apoptosis in view of p53 and Bak, caspase-9 and caspase-3 enhancement, and Bcl2 downregulation [96]

Further, in a mouse model of Alzheimer's disease, NMN was found to reduce the levels of amyloid precursor protein (APP), reverse the oxygen consumption deficit in brain mitochondria, and reduce mitochondrial fragmentation in neurons, thereby improving the mitochondrial respiratory defect [40]

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This protein can create an iron-overloaded environment and lay the foundation for the occurrence of cellular ferroptosis

L., & Magrina, J

Compare that to vitamins taken orally, with an average absorption rate of 10%