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Open AccessJournal ArticleDOI

NAD+ in Aging: Molecular Mechanisms and Translational Implications

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TLDR
Technological and pharmacological interventions bolstering cellular NAD+ levels might retard aspects of aging and forestall some age-related diseases.
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This article is published in Trends in Molecular Medicine.The article was published on 2017-10-01 and is currently open access. It has received 287 citations till now. The article focuses on the topics: NAD+ kinase.

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Ageing as a risk factor for neurodegenerative disease.

TL;DR: Hallmarks of ageing — genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication — correlate with susceptibility to neurodegenerative disease.
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Tryptophan metabolism as a common therapeutic target in cancer, neurodegeneration and beyond

TL;DR: An overview of the physiological and pathophysiological roles of tryptophan metabolism is provided, focusing on the clinical potential and challenges associated with targeting this pathway.
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Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States.

TL;DR: An overview of the cellular and molecular biology of brain aging, how those processes interface with disease-specific neurodegenerative pathways, and how metabolic states influence brain health is provided.
Journal ArticleDOI

NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR

TL;DR: A comprehensive concept that connects NAD+ metabolism to the control of aging and longevity in mammals has been proposed, and the stage is now set to test whether these exciting preclinical results can be translated to improve human health.
References
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Journal ArticleDOI

The Hallmarks of Aging

TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
Journal ArticleDOI

Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1

TL;DR: PGC-1, a cold-inducible coactivator of nuclear receptors, stimulates mitochondrial biogenesis and respiration in muscle cells through an induction of uncoupling protein 2 (UCP-2) and through regulation of the nuclear respiratory factors (NRFs).
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AMPK regulates energy expenditure by modulating NAD + metabolism and SIRT1 activity

TL;DR: It is demonstrated that AMPK controls the expression of genes involved in energy metabolism in mouse skeletal muscle by acting in coordination with another metabolic sensor, the NAD+-dependent type III deacetylase SIRT1.
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