ReviewJournal of Alzheimer's disease : JAD2023
DNA Damage Response-Associated Cell Cycle Re-Entry and Neuronal Senescence in Brain Aging and Alzheimer's Disease.
Review in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed.
- Desflurane Increases Hippocampal RAF-MAPK-MSK1 Protein Levels and Reduces CLOCK Expression: Sorafenib Attenuates Cognitive Impairment in Aged Mice.Neurochemical research · 2026Article
- Coincidence of L1 retrotransposition and DNA repair deficiency elicits synthetic lethality in S-phase mature neurons.iScience · 2026Article
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Blood-based proteomic signature of amyloidosis: identification of novel regulators of amyloid load.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- MYC-driven gliosis impairs neuron-glia communication in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- Differential Gene Expression in Human Hippocampus With Aging.Aging cell · 2026Article
- Review
- The relationship between DNA damage and repair and the occurrence and development of disease.Frontiers in genetics · 2026Review
- Review
- Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.Antioxidants (Basel, Switzerland) · 2025Review
- Multi-modal investigation reveals pathogenic features of diverse DDX3X missense mutations.PLoS genetics · 2025Article
- Ezh2 Delays Activation of Differentiation Genes During Normal Cerebellar Granule Neuron Development and in Medulloblastoma.bioRxiv : the preprint server for biology · 2024Article
- Cholesterol Accumulation Promotes Photoreceptor Senescence and Retinal Degeneration.Investigative ophthalmology & visual science · 2024Article
- Neuronal cell cycle reentry events in the aging brain are more prevalent in neurodegeneration and lead to cellular senescence.PLoS biology · 2024Article
- Extracellular vesicles from human urine-derived stem cells delay aging through the transfer of PLAU and TIMP1.Acta pharmaceutica Sinica. B · 2024Article
- Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures.GeroScience · 2023Review
- Neuropathological Examination of Mice Chronically Exposed to Secondhand Smoke.Military medicine · 2023Article
- Influence of N6-methyladenosine (m6A) modification on cell phenotype in Alzheimer's disease.PloS one · 2023Article
- Introduction to The Special Issue: Novel Molecular Pathways and Therapeutic Challenges in Neurodegenerative Diseases.Journal of Alzheimer's disease : JAD · 2023Article
- Interchromosomal translocation in neural progenitor cells exposed to L1 retrotransposition.Genetics and molecular biology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronological aging is by far the strongest risk factor for age-related dementia and Alzheimer's disease. Senescent cells accumulated in the aging and Alzheimer's disease brains are now recognized as the keys to describing such an association. Cellular senescence is a classic phenomenon characterized by stable cell arrest, which is thought to be applicable only to dividing cells. Emerging evidence indicates that fully differentiated post-mitotic neurons are also capable of becoming senescent, with roles in contributing to both brain aging and disease pathogenesis. The key question that arises is the identity of the upstream triggers and the molecular mechanisms that underly such changes. Here, we highlight the potential role of persistent DNA damage response as the major driver of senescent phenotypes and discuss the current evidence and molecular mechanisms that connect DNA repair infidelity, cell cycle re-entry and terminal fate decision in committing neuronal cell senescence.
Indexed as
Identifiers
What Socratic 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 Socratic graph.