ArticleNeurobiology of disease2012
Loss of circadian clock accelerates aging in neurodegeneration-prone mutants.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
56 citing papers in PubMed, 102 citations in OpenAlex.
- Bidirectional Mechanisms Linking Circadian Rhythm Disruption and Parkinson's Disease: Chronobiomarkers and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Circadian clock regulation in lung health and disease: molecular mechanisms and therapeutic opportunities.EXCLI journal · 2026Review
- Multifaceted dynamics of circadian timing system influence aging and longevity.Biogerontology · 2025Review
- Artificial light at night accelerates aging processes in pre-pubertal female rats.Biogerontology · 2025Article
- Enhanced Age-Dependent Motor Impairment in Males ofBiology · 2024Article
- DEC1 is involved in circadian rhythm disruption-exacerbated pulmonary fibrosis.Cell communication and signaling : CCS · 2024Article
- Article
- 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
- Hsp40 overexpression in pacemaker neurons delays circadian dysfunction in a Drosophila model of Huntington's disease.Disease models & mechanisms · 2022Article
- RCAN1 knockout and overexpression recapitulate an ensemble of rest-activity and circadian disruptions characteristic of Down syndrome, Alzheimer's disease, and normative aging.Journal of neurodevelopmental disorders · 2022Article
- Discovery and Visualization of Age-Dependent Patterns in the Diurnal Transcriptome of Drosophila.Journal of circadian rhythms · 2022Article
- Empowering Melatonin Therapeutics withDiseases (Basel, Switzerland) · 2021Review
- The Molecular Clock and Neurodegenerative Disease: A Stressful Time.Frontiers in molecular biosciences · 2021Review
- Circadian Rhythm Disruption and Alzheimer's Disease: The Dynamics of a Vicious Cycle.Current neuropharmacology · 2021Article
- Understanding the Emerging Link Between Circadian Rhythm, Nrf2 Pathway, and Breast Cancer to Overcome Drug Resistance.Frontiers in pharmacology · 2021Review
- (-)-Epigallocatechin-3-gallate Ameliorates Intervertebral Disc Degeneration Through Reprogramming of the Circadian Clock.Frontiers in pharmacology · 2021Article
- Loss of function in the Drosophila clock gene period results in altered intermediary lipid metabolism and increased susceptibility to starvation.Cellular and molecular life sciences : CMLS · 2020Article
- The wrinkling of time: Aging, inflammation, oxidative stress, and the circadian clock in neurodegeneration.Neurobiology of disease · 2020Review
- Molecular mechanisms and physiological importance of circadian rhythms.Nature reviews. Molecular cell biology · 2020Review
- Aging and the clock: Perspective from flies to humans.The European journal of neuroscience · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Circadian clocks generate rhythms in molecular, cellular, physiological, and behavioral processes. Recent studies suggest that disruption of the clock mechanism accelerates organismal senescence and age-related pathologies in mammals. Impaired circadian rhythms are observed in many neurological diseases; however, it is not clear whether loss of rhythms is the cause or result of neurodegeneration, or both. To address this important question, we examined the effects of circadian disruption in Drosophila melanogaster mutants that display clock-unrelated neurodegenerative phenotypes. We combined a null mutation in the clock gene period (per(01)) that abolishes circadian rhythms, with a hypomorphic mutation in the carbonyl reductase gene sniffer (sni(1)), which displays oxidative stress induced neurodegeneration. We report that disruption of circadian rhythms in sni(1) mutants significantly reduces their lifespan compared to single mutants. Shortened lifespan in double mutants was coupled with accelerated neuronal degeneration evidenced by vacuolization in the adult brain. In addition, per(01)sni(1) flies showed drastically impaired vertical mobility and increased accumulation of carbonylated proteins compared to age-matched single mutant flies. Loss of per function does not affect sni mRNA expression, suggesting that these genes act via independent pathways producing additive effects. Finally, we show that per(01) mutation accelerates the onset of brain pathologies when combined with neurodegeneration-prone mutation in another gene, swiss cheese (sws(1)), which does not operate through the oxidative stress pathway. Taken together, our data suggest that the period gene may be causally involved in neuroprotective pathways in aging Drosophila.
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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.