Extension of Lifespan and Amelioration of Alzheimer's Disease Phenotypes by Genetic Manipulation of Mitochondrial NAD

Suman Rimal, Jae-Hyuk Lee, Yanzi He, Bingwei Lu

Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA. · pubmed

Paper

Abstract

Aging remains the most significant risk factor for common neurodegenerative diseases including Alzheimer's disease (AD). According to the geroscience hypothesis, aging is malleable and that by targeting basic aging physiology, we can alleviate many of the age-related chronic diseases. The common mechanisms driving aging and age-related diseases remain poorly defined. Mitochondrial dysfunction is recognized as a fundamental hallmark of aging, and recent studies implicate mitochondrial reverse electron transport (RET) as a driver of aging. The key outcomes of RET, increased ROS and decreased NAD

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Research summary

The paper claims that genetic manipulation of mitochondrial NAD can extend lifespan and improve Alzheimer's disease phenotypes. This research addresses the underlying mechanisms of aging and their relationship to age-related diseases, aligning with the goal of targeting aging physiology to mitigate chronic diseases.

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