ArticleMolecular neurodegeneration2024
Rejuvenating aged microglia by p16
Article in Molecular neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice.Nature communications · 2026Article
- Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.iScience · 2026Article
- Brain-targeted delivery of siRNA via non-viral delivery systems, the therapeutic strategy for Alzheimer's disease-Unveiling challenges and prospects.International journal of pharmaceutics: X · 2026Review
- Viral Mimicry of Alzheimer's Disease: Innate Sensing of Self-Nucleic Acids as a Driver of Glial Senescence.Journal of molecular neuroscience : MN · 2026Review
- PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.Experimental neurobiology · 2026Article
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- Advancements in nanomedicine for the therapeutic regulation of efferocytosis: opportunities and challenges.Theranostics · 2026Review
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- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Top-down engineered micron-cell derived nanovesicles encapsulating curcumin targeting the 3R strategy (remove, remodel, repair) for Alzheimer's disease therapy.Materials today. Bio · 2025Article
- Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- The Multifaceted Role of Extracellular Vesicles in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- The Application of Polymeric Nanoparticles as Drug Delivery Carriers to Cells in Neurodegenerative Diseases.Cell proliferation · 2025Review
- The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025Review
- Elevated p16Ink4a Expression Enhances Tau Phosphorylation in Neurons Differentiated From Human-Induced Pluripotent Stem Cells.Aging cell · 2025Article
- PLGA nanoparticle-mediated anti-inflammatory gene delivery for the treatment of neuropathic pain.Nanomedicine (London, England) · 2025Article
- Nanoscale drug formulations for the treatment of Alzheimer's disease progression.RSC advances · 2025Review
- Engineered nanoparticles for the treatment of Alzheimer's disease.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 8 institutions in 2 countries.
Funding
Abstract
Age-dependent accumulation of amyloid plaques in patients with sporadic Alzheimer's disease (AD) is associated with reduced amyloid clearance. Older microglia have a reduced ability to phagocytose amyloid, so phagocytosis of amyloid plaques by microglia could be regulated to prevent amyloid accumulation. Furthermore, considering the aging-related disruption of cell cycle machinery in old microglia, we hypothesize that regulating their cell cycle could rejuvenate them and enhance their ability to promote more efficient amyloid clearance. First, we used gene ontology analysis of microglia from young and old mice to identify differential expression of cyclin-dependent kinase inhibitor 2A (p16
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.