Cited by 501Sirtuins and Resveratrol in MedicineBiochemical and Molecular ResearchGenetics, Aging, and Longevity in Model Organisms

The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.

NAD(+) in aging: molecular mechanisms and translational implications

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Abstract

The coenzyme NAD+ is critical in cellular bioenergetics and adaptive stress responses. Its depletion has emerged as a fundamental feature of aging that may predispose to a wide range of chronic diseases. Maintenance of NAD+ levels is important for cells with high energy demands and for proficient neuronal function. NAD+ depletion is detected in major neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases, cardiovascular disease and muscle atrophy. Emerging evidence suggests that NAD+ decrements occur in various tissues during aging, and that physiological and pharmacological interventions bolstering cellular NAD+ levels might retard aspects of aging and forestall some age-related diseases. Here, we discuss aspects of NAD+ biosynthesis, together with putative mechanisms of NAD+ action against aging, including recent preclinical and clinical trials.

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Crossref · 10.1016/j.molmed.2017.08.001

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Research works printed but not linked: 5

  1. Verdin, 2015, NAD(+) in aging, metabolism, and neurodegeneration, Science, 350, 1208, 10.1126/science.aac4854 · DOI · Paper page
  2. Kerr, 2017, Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms, Trends Neurosci., 40, 151, 10.1016/j.tins.2017.01.002 · DOI · Paper page
  3. Scheibye-Knudsen, 2014, A high fat diet and NAD+ rescue premature aging in cockayne syndrome, Cell Metab., 20, 840, 10.1016/j.cmet.2014.10.005 · DOI · Paper page
  4. Fang, 2016, Nuclear DNA damage signalling to mitochondria in ageing, Nat. Rev. Mol. Cell Biol., 17, 308, 10.1038/nrm.2016.14 · DOI · Paper page
  5. Fang, 2016, NAD+ replenishment improves lifespan and healthspan in ataxia telangiectasia models via mitophagy and DNA repair, Cell Metab., 24, 566, 10.1016/j.cmet.2016.09.004 · DOI · Paper page

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Metadata

Authors
Fang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., & Bohr, V. A.
Affiliations
  • National Institutes of Health (US)
  • University of Copenhagen (DK)
Corresponding author
Bohr, Vilhelm A.
Venue
Trends in Molecular Medicine
Publisher
Elsevier BV
Published
2017-10
Volume
23
Issue
10
Pages
899-916
ISSN
1471-4914 (ISSN-L)
OpenAlex
W2751352835
Cited by
501
References
119
Citations by year
2026: 42 · 2025: 75 · 2024: 69 · 2023: 45 · 2022: 64 · 2021: 74 · 2020: 53 · 2019: 48 · 2018: 29 · 2017: 2
FWCI
4.13
Type
journal article
Language
en
Open access
Locations
  • Trends in Molecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • NORA - Norwegian Open Research Archives (submittedVersion, other-oa)
  • NORA - Norwegian Open Research Archives (submittedVersion, cc-by-nc-nd)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
  • Scopus (Elsevier) (submittedVersion)
Funders
  • Intramural Research Program of the National Institute on Aging (2015-2016, 2016-2017)
  • The Oticon Foundation
  • Ib Henriksen’s Foundation
Topics
  • Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
NAD+, aging, NAD+ depletion, NAD biosynthesis, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, cardiovascular disease, muscle atrophy, age-related diseases, NAD+ supplementation, cellular bioenergetics, stress response
MeSH terms
Aging, Alzheimer Disease, Animals, Cardiovascular Diseases, Energy Metabolism, Humans, Muscular Atrophy, NAD, Parkinson Disease

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