ArticleAging2009
The circadian clock gene period extends healthspan in aging Drosophila melanogaster.
Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 147 citations in OpenAlex.
- PARK(ing) time-How park deficiency affects the biological clock in a Drosophila model of Parkinson's disease.FEBS letters · 2026Article
- Multifaceted dynamics of circadian timing system influence aging and longevity.Biogerontology · 2025Review
- Capturing continuous, long timescale behavioral changes in Drosophila melanogaster postural data.PLoS computational biology · 2025Article
- Circadian Rhythm Dysfunction in Neurodegenerative Diseases: A Bidirectional Perspective and Therapeutic Potential.Nature and science of sleep · 2025Review
- Article
- LKRSDH-dependent histone modifications of insulin-like peptide sites contribute to age-related circadian rhythm changes.Nature communications · 2024Article
- Glial lipid droplets resolve ROS during sleep.Nature neuroscience · 2024Article
- The contribution of circadian clock to the biological processes.Frontiers in molecular biosciences · 2024Review
- Article
- Circadian clock disruption promotes the degeneration of dopaminergic neurons in male Drosophila.Nature communications · 2023Article
- What do we mean by "aging"? Questions and perspectives revealed by studies in Drosophila.Mechanisms of ageing and development · 2023Article
- Evaluating the Genetic Role of Circadian Clock Genes in Parkinson's Disease.Molecular neurobiology · 2023Article
- Stable Expression of dmiR-283 in the Brain Promises Positive Effects in Endurance Exercise on Sleep-Wake Behavior in AgingInternational journal of molecular sciences · 2023Article
- Markers and mechanisms of death inFrontiers in aging · 2023Article
- Chronic exposure to dim light at night disrupts cell-mediated immune response and decreases longevity in aged female mice.Chronobiology international · 2022Article
- WNT/β-catenin pathway and circadian rhythms in obsessive-compulsive disorder.Neural regeneration research · 2022Review
- Circadian Control of Mitochondria in Reactive Oxygen Species Homeostasis.Antioxidants & redox signaling · 2022Review
- Article
- Circadian Clocks, Redox Homeostasis, and Exercise: Time to Connect the Dots?Antioxidants (Basel, Switzerland) · 2022Review
- Possible actions of cannabidiol in obsessive-compulsive disorder by targeting the WNT/β-catenin pathway.Molecular psychiatry · 2022Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
There is increasing evidence that aging is affected by biological (circadian) clocks - the internal mechanisms that coordinate daily changes in gene expression, physiological functions and behavior with external day/night cycles. Recent data suggest that disruption of the mammalian circadian clock results in accelerated aging and increased age-related pathologies such as cancer; however, the links between loss of daily rhythms and aging are not understood. We sought to determine whether disruption of the circadian clock affects lifespan and healthspan in the model organism Drosophila melanogaster. We examined effects of a null mutation in the circadian clock gene period (per(01)) on the fly healthspan by challenging aging flies with short-term oxidative stress (24h hyperoxia) and investigating their response in terms of mortality hazard, levels of oxidative damage, and functional senescence. Exposure to 24h hyperoxia during middle age significantly shortened the life expectancy in per(01) but not in control flies. This homeostatic challenge also led to significantly higher accumulation of oxidative damage in per(01) flies compared to controls. In addition, aging per(01) flies showed accelerated functional decline, such as lower climbing ability and increased neuronal degeneration compared to age-matched controls. Together, these data suggest that impaired stress defense pathways may contribute to accelerated aging in the per mutant. In addition, we show that the expression of per gene declines in old wild type flies, suggesting that the circadian regulatory network becomes impaired with age.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.