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Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model
BackgroundMitochondrial dysfunction is a hallmark of neurodegenerative diseases including Alzheimer’s disease (AD), with morphological and functional abnormalities limiting the electron transportExpand
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Mitochondrial NUDIX hydrolases: A metabolic link between NAD catabolism, GTP and mitochondrial dynamics
&NA; NAD+ catabolism and mitochondrial dynamics are important parts of normal mitochondrial function and are both reported to be disrupted in aging, neurodegenerative diseases, and acute brainExpand
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NAD+ precursor modulates post-ischemic mitochondrial fragmentation and reactive oxygen species generation via SIRT3 dependent mechanisms
Global cerebral ischemia depletes brain tissue NAD+, an essential cofactor for mitochondrial and cellular metabolism, leading to bioenergetics failure and cell death. The post-ischemic NAD+ levelsExpand
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Significance of Mitochondrial Protein Post-translational Modifications in Pathophysiology of Brain Injury
Mitochondria are complex organelles that undergo constant fusion and fission in order to adapt to the ever-changing cellular environment. The fusion/fission proteins, localized in the inner and outerExpand
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Nicotinamide mononucleotide alters mitochondrial dynamics by SIRT3‐dependent mechanism in male mice
Nicotinamide adenine dinucleotide (NAD+) is a central signaling molecule and enzyme cofactor that is involved in a variety of fundamental biological processes. NAD+ levels decline with age,Expand
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Interplay between NAD+ and acetyl‑CoA metabolism in ischemia-induced mitochondrial pathophysiology.
Brain injury caused by ischemic insult due to significant reduction or interruption in cerebral blood flow leads to disruption of practically all cellular metabolic pathways. This triggers a complexExpand
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