ArticleCell stem cell2022
Increased post-mitotic senescence in aged human neurons is a pathological feature of Alzheimer's disease.
Article in Cell stem cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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Who cites it
144 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- Direct Conversion of Fibroblast into Neurons for Alzheimer's Disease Research: A Systematic Review.Journal of Alzheimer's disease : JAD · 2023Pooled it
- Review
- Beyond phenotypic markers: rethinking dopaminergic identity in iPSC-derived neurons.Cell communication and signaling : CCS · 2026Review
- Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence.Aging cell · 2026Review
- Acetyl L-Carnitine Nanoparticles Modulate Neuronal and Inflammatory Responses in In Vitro Cell Model.International journal of molecular sciences · 2026Article
- Review
- LncRNA DLX6-AS1 Regulates the Pathological Process Related to Alzheimer's Disease via miR-204-5p.Neuromolecular medicine · 2026Article
- Single-cell multiomics connects 3D genome and transcriptome alterations in Alzheimer's disease.Science (New York, N.Y.) · 2026Article
- APOE4 disrupts the central dogma by arresting neuronal proteome dynamics.bioRxiv : the preprint server for biology · 2026Article
- Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.Journal of neuroinflammation · 2026Article
- Microglial checkpoint collapse in Alzheimer's disease: a tri-axial framework for biomarker-informed neuroimmune therapy.Journal of neuroinflammation · 2026Review
- Exploring Stem Cell Based Senotherapeutic Strategies for Targeting Cellular Senescence in Brain Aging.Stem cell reviews and reports · 2026Review
- Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.iScience · 2026Article
- Sex-linked helicases DDX3X and DDX3Y regulate G-quadruplex-associated stress in neurons.Cell death & disease · 2026Article
- Repurposing niclosamide to mitigate inflammaging: a review of multi-target mechanisms in cellular senescence and age-related decline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Review
- Cellular senescence as a therapeutic target for aging intervention.Biomedical journal · 2026Review
- Investigating the Causal Links between the Aging Process and Alzheimer's Disease Pathogenesis.International journal of stem cells · 2026Review
- Psychosis as a multisystem disorder of aberrant aging.npj aging · 2026Review
- Selective elimination of amyloid-β-induced senescent neuroblastoma cells by Moringa oleifera leaf extract.Scientific reports · 2026Article
84 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
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The concept of senescence as a phenomenon limited to proliferating cells has been challenged by growing evidence of senescence-like features in terminally differentiated cells, including neurons. The persistence of senescent cells late in life is associated with tissue dysfunction and increased risk of age-related disease. We found that Alzheimer's disease (AD) brains have significantly higher proportions of neurons that express senescence markers, and their distribution indicates bystander effects. AD patient-derived directly induced neurons (iNs) exhibit strong transcriptomic, epigenetic, and molecular biomarker signatures, indicating a specific human neuronal senescence-like state. AD iN single-cell transcriptomics revealed that senescent-like neurons face oncogenic challenges and metabolic dysfunction as well as display a pro-inflammatory signature. Integrative profiling of the inflammatory secretome of AD iNs and patient cerebral spinal fluid revealed a neuronal senescence-associated secretory phenotype that could trigger astrogliosis in human astrocytes. Finally, we show that targeting senescence-like neurons with senotherapeutics could be a strategy for preventing or treating AD.
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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.