A high-fat diet and NAD(+) activate Sirt1 to rescue premature aging in Cockayne syndrome
Open accessAbstract
Cockayne syndrome (CS) is an accelerated aging disorder characterized by progressive neurodegeneration caused by mutations in genes encoding the DNA repair proteins CS group A or B (CSA or CSB). Since dietary interventions can alter neurodegenerative processes, Csb(m/m) mice were given a high-fat, caloric-restricted, or resveratrol-supplemented diet. High-fat feeding rescued the metabolic, transcriptomic, and behavioral phenotypes of Csb(m/m) mice. Furthermore, premature aging in CS mice, nematodes, and human cells results from aberrant PARP activation due to deficient DNA repair leading to decreased SIRT1 activity and mitochondrial dysfunction. Notably, β-hydroxybutyrate levels are increased by the high-fat diet, and β-hydroxybutyrate, PARP inhibition, or NAD(+) supplementation can activate SIRT1 and rescue CS-associated phenotypes. Mechanistically, CSB can displace activated PARP1 from damaged DNA to limit its activity. This study connects two emerging longevity metabolites, β-hydroxybutyrate and NAD(+), through the deacetylase SIRT1 and suggests possible interventions for CS.
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NAD+ depletion occurs in accelerated aging diseases with neurodegeneration, including ataxia telangiectasia, xeroderma pigmentosum group A, and Cockayne syndrome.
“Several accelerated aging diseases exhibit neurodegeneration, including ataxia telangiectasia (AT), xeroderma pigmentosum group A (XPA), and Cockayne syndrome (CS). NAD+ depletion has been shown in both C. elegans and brain tissues from mouse models of AT, XPA, and CS.”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Scheibye-Knudsen et al., 2014
NAD+ augmentation strategies, including NR or NMN, PARP1 inhibitor, or SIRT1 activator, improve healthspan and lifespan in accelerated aging animal models.
“In line with the importance of NAD+ depletion in neurodegeneration, multiple NAD+ augmentation strategies (including treatment with the NAD+ precursors NR or NMN, or treatment with a PARP1 inhibitor or a SIRT1 activator) improved healthspan and lifespan in the accelerated aging animal models (Fang et al., 2014, 2016a; Scheibye-Knudsen et al., 2014).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Scheibye-Knudsen et al., 2014
NAD+ augmentation decreases elevated ROS in cell and animal models of premature aging through reduced ROS production, improved mitochondrial function, and possibly increased ROS detoxification.
“Moreover, NAD+ augmentation decreases the elevated levels of ROS in cell and animal models of premature aging diseases through reduced ROS production, improved mitochondrial function, and possibly also increased ROS detoxification (Fang et al., 2016a, 2019; Scheibye-Knudsen et al., 2014).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Scheibye-Knudsen et al., 2014
Reduced NAD+ levels play a pivotal role in brain aging and neurodegenerative disorders because NAD+ replenishment improves mitochondrial function and biogenesis and reduces damaged mitochondria in premature aging and Alzheimer's disease models.
“Reduced NAD+ levels play a pivotal role in brain aging and neurodegenerative disorders because NAD+ replenishment improves mitochondrial function and mitochondrial biogenesis and reduces accumulation of damaged mitochondria in both premature aging models and Alzheimer’s disease (AD) models (Fang et al., 2014, 2016a; Scheibye-Knudsen et al., 2014).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Scheibye-Knudsen et al., 2014
NAD+ depletion is reported in several models of accelerated ageing that exhibit neurodegeneration, as well as in neurodegenerative diseases including Alzheimer disease, Parkinson disease and amyotrophic lateral sclerosis.
“NAD+ depletion is reported in several models of accelerated ageing which exhibit neurodegeneration33,134,135, as well as in neuro-degenerative diseases, including Alzheimer disease136, Parkinson disease137,138 and amyotrophic lateral sclerosis (ALS)139.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [33]
NAD+ replenishment using NR and/or NMN delays progeroid phenotype and extends lifespan in C. elegans models of xeroderma pigmentosum group A, ataxia telangiectasia and Cockayne syndrome, and in a worm model of Werner syndrome.
“NAD+ replenishment, using NR and/or NMN, has also been effective in delaying progeroid phenotype and extending lifespan in relevant C. elegans models of xeroderma pigmentosum group A, ataxia telangiectasia and Cockayne syndrome33,134,135 and in a worm model of Werner syndrome (a progeroid disease)196.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [33]
In these models, supplying NAD+ pharmacologically or blocking PARP1 restores SIRT1 activity and mitochondrial homeostasis.
“Pharmacological NAD+ supplementation or inhibition of PARP1 was able to re-establish SIRT1 activity and recover mitochondrial homeostasis85,86.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [86]
Animal models and patient-derived cells for xeroderma pigmentosum and Cockayne syndrome show lower SIRT1 activity and sustained PARP activation caused by unrepaired DNA damage.
“Additionally, studies conducted in animal models and cells derived from people affected by xeroderma pigmentosum and Cockayne syndrome found decreased SIRT1 activity and persistent PARP activation due to unrepaired DNA damage.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [86]
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- Authors
- Scheibye-Knudsen, M., Mitchell, S. J., Fang, E. F., Iyama, T., Ward, T., Wang, J., Dunn, C. A., Singh, N., Veith, S., Hasan-Olive, M. M., Mangerich, A., Wilson, M. A., Mattson, M. P., Bergersen, L. H., Cogger, V. C., Warren, A., Le Couteur, D. G., Moaddel, R., Wilson, D. M., Croteau, D. L., de Cabo, R., & Bohr, V. A.
- Affiliations
- The University of Sydney (AU)
- National Institutes of Health (US)
- University of Konstanz (DE)
- University of Copenhagen (DK)
- Corresponding author
- Bohr, Vilhelm A.
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 20
- Issue
- 5
- Pages
- 840-855
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC4261735
- OpenAlex
- W2076252987
- Cited by
- 352
- References
- 29
- Citations by year
- 2026: 10 · 2025: 27 · 2024: 20 · 2023: 24 · 2022: 43 · 2021: 43 · 2020: 38 · 2019: 30 · 2018: 40 · 2017: 28 · 2016: 29 · 2015: 18 · 2014: 1
- FWCI
- 12.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (ZIAAG000368, ZIAAG000363)
- Topics
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- Cockayne syndrome, premature aging, SIRT1, NAD+, high-fat diet, caloric restriction, resveratrol, beta-hydroxybutyrate, PARP1, DNA repair, CSB, mitochondrial dysfunction, neurodegeneration, dietary intervention
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, Animals, Cell Line, Cockayne Syndrome, Enzyme Activation, Humans, Mice, Inbred C57BL, Mitochondria, NAD, Poly(ADP-ribose) Polymerases, Aging, Premature, 3-Hydroxybutyric Acid, Mice, Sirtuin 1, Diet, High-Fat
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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