ArticleAging cell2013
Lifespan extension by dietary intervention in a mouse model of Cockayne syndrome uncouples early postnatal development from segmental progeria.
Article in Aging cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- AAV-mediated gene therapy demonstrates phenotypic rescue in a mouse model of Cockayne syndrome.The Journal of clinical investigation · 2026Article
- Pharmacologic AMPK Activation Extends Lifespan inbioRxiv : the preprint server for biology · 2026Article
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- Premature aging in genetic diseases: what conclusions can be drawn for physiological aging.Frontiers in aging · 2023Review
- Body Composition and Metabolic Changes in a Lyon Hypertensive Congenic Rat and Identification ofFrontiers in genetics · 2022Article
- DNA repair-related genes and adipogenesis: Lessons from congenital lipodystrophies.Genetics and molecular biology · 2022Article
- Intracellular HCell chemical biology · 2021Article
- Article
- Cockayne Syndrome: The many challenges and approaches to understand a multifaceted disease.Genetics and molecular biology · 2020Article
- Article
- Function and Interactions of ERCC1-XPF in DNA Damage Response.Molecules (Basel, Switzerland) · 2018Review
- Cockayne syndrome: Clinical features, model systems and pathways.Ageing research reviews · 2017Review
- Increased oxidative phosphorylation in response to acute and chronic DNA damage.NPJ aging and mechanisms of disease · 2016Article
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
- The cockayne syndrome B protein is essential for neuronal differentiation and neuritogenesis.Cell death & disease · 2014Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cockayne syndrome (CS) is a rare autosomal recessive segmental progeria characterized by growth failure, lipodystrophy, neurological abnormalities, and photosensitivity, but without skin cancer predisposition. Cockayne syndrome life expectancy ranges from 5 to 16 years for the two most severe forms (types II and I, respectively). Mouse models of CS have thus far been of limited value due to either very mild phenotypes, or premature death during postnatal development prior to weaning. The cause of death in severe CS models is unknown, but has been attributed to extremely rapid aging. Here, we found that providing mutant pups with soft food from as late as postnatal day 14 allowed survival past weaning with high penetrance independent of dietary macronutrient balance in a novel CS model (Csa(-/-) | Xpa(-/-)). Survival past weaning revealed a number of CS-like symptoms including small size, progressive loss of adiposity, and neurological symptoms, with a maximum lifespan of 19 weeks. Our results caution against interpretation of death before weaning as premature aging, and at the same time provide a valuable new tool for understanding mechanisms of progressive CS-related progeroid symptoms including lipodystrophy and neurodysfunction.
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Registered trials
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