ReviewNature communications2023
An aging, pathology burden, and glial senescence build-up hypothesis for late onset Alzheimer's disease.
Review in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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
99 citing papers in PubMed, 155 citations in OpenAlex.
- Sex-specific regulation of angiogenin in Alzheimer's disease.Molecular psychiatry · 2026Article
- Astrocytes in Neurodegeneration: Spatial States, Crosstalk, and Emerging Therapies.Molecular neurobiology · 2026Review
- Genetic Deletion of Adenosine AGlia · 2026Article
- uPAR exhibits age- and region-dependent expression in the brains of mice with Alzheimer's disease-like pathology.Brain research · 2026Article
- Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice.Nature communications · 2026Article
- Single-cell multiomics connects 3D genome and transcriptome alterations in Alzheimer's disease.Science (New York, N.Y.) · 2026Article
- DNA Sensing and Neuroinflammation: Mechanistic Insights into cGAS-STING Biology and Therapeutic Translation in Age-Related Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Review
- Reprogramming Neuroinflammation: Mitochondrial Targets and Immune Checkpoint Inhibitors in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Andrographolide attenuates microglial senescence in Alzheimer's disease mice by suppressing the STAT3 signaling.iScience · 2026Article
- TPM1 drives cytoskeleton-immunometabolism coupling and LGALS9/CD45-mediated neuroinflammatory propagation in retinitis pigmentosa.Science advances · 2026Article
- Immune involvement in neuropsychiatric disorders: Insights from single-cell transcriptomic studies.Psychiatry and clinical neurosciences · 2026Review
- Variations in perfusion detectable in advance of microstructure in white matter aging.GeroScience · 2026Article
- Article
- When Alzheimer's pathology meets cardiometabolic risk: intrinsic subcortical-cortical connectivity signatures of retroactive interference in aging.Alzheimer's research & therapy · 2026Article
- The Role of Microglial Cells and Cytokine Modulation in Alzheimer's Disease: A Neuroinflammatory Perspective.Current Alzheimer research · 2026Review
- Cellular senescence in brain aging and neurodegeneration: from molecular mechanisms to translational opportunities.Frontiers in cellular neuroscience · 2026Review
- Neurosenescence, inflammaging and neuroinflammation in neurodegenerative disorders.Frontiers in aging · 2026Review
- Introducing Cellular Senescence in Human Induced Pluripotent Stem Cells and Differentiated Neural Lineage for Modeling of Age-Associated Diseases.Advanced biology · 2026Article
- ZNF865 (BLST) Regulates Back Pain via Cell Senescence and DNA Damage Mechanisms.bioRxiv : the preprint server for biology · 2025Article
39 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
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) predominantly occurs as a late onset (LOAD) form involving neurodegeneration and cognitive decline with progressive memory loss. Risk factors that include aging promote accumulation of AD pathologies, such as amyloid-beta and tau aggregates, as well as inflammation and oxidative stress. Homeostatic glial states regulate and suppress pathology buildup; inflammatory states exacerbate pathology by releasing pro-inflammatory cytokines. Multiple stresses likely induce glial senescence, which could decrease supportive functions and reinforce inflammation. In this perspective, we hypothesize that aging first drives AD pathology burden, whereafter AD pathology putatively induces glial senescence in LOAD. We hypothesize that increasing glial senescence, particularly local senescent microglia accumulation, sustains and drives perpetuating buildup and spread of AD pathologies, glial aging, and further senescence. We predict that increasing glial senescence, particularly local senescent microglia accumulation, also transitions individuals from healthy cognition into mild cognitive impairment and LOAD diagnosis. These pathophysiological underpinnings may centrally contribute to LOAD onset, but require further mechanistic investigation.
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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.