ReviewActa neuropathologica communications2014
Microglial pathology.
Review in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 3 of them syntheses that pooled it.
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
184 citing papers in PubMed, 3 syntheses or guidelines pooled it, 317 citations in OpenAlex.
- Shaping the future of preclinical development of successful disease-modifying drugs against Alzheimer's disease: a systematic review of tau propagation models.Acta neuropathologica communications · 2024Pooled it
- Pooled it
- The Amyloid-β Pathway in Alzheimer's Disease.Molecular psychiatry · 2021Pooled it
- Human amniotic mesenchymal stromal cell-derived extracellular vesicles reprogram microglia and prevent neurodegeneration in experimental models of Alzheimer's disease.Translational neurodegeneration · 2026Article
- Palmitoylethanolamide and Luteolin in Brain Aging and Cognitive Decline: Biological Rationale and Current Evidence.Nutrients · 2026Review
- Aurka-Bhlhe41 axis prevents premature aging-like microglial dysfunction and promotes remyelination.Nature communications · 2026Article
- Targeting the Biology of Aging in Cerebrovascular Disease: Inflammation, Metabolism, Senescence, and Regeneration.International journal of molecular sciences · 2026Review
- The functional role of glial cells in the pathologic brain as reviewed by Alois Alzheimer in 1910.Molecular neurodegeneration · 2026Article
- Gut Microbiota and Interorgan Communication Among the Gut, Brain, and Beyond.Internal medicine (Tokyo, Japan) · 2026Review
- Diet-Driven Microglial Activation: Region-Specific Neuroinflammation in the Mouse Brain.Brain sciences · 2025Article
- Therapeutic Potentials of the Seaweed-Derived Compounds for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Exploring the Impact of a High-Fat Diet on Brain Homeostasis: A Comprehensive Analysis of the Absence of Inflammation.Molecular nutrition & food research · 2025Article
- Microglia interact with dendritic spines and regulate spine numbers after brain injury following resuscitation from a cardiac arrest.Experimental neurology · 2025Article
- A disproportionality analysis of adverse events caused by pexidartinib from the FDA adverse event reporting system.Scientific reports · 2025Article
- Probiotic Supplementation Improves the Clinical Measures of Cognition in Patients With Mild Cognitive Impairment.Cureus · 2025Review
- Microglial Dystrophy and Spatial Learning Impairments Following Exposure to Multiple Early-life Stressors in Rats.Annals of neurosciences · 2025Article
- Extracellular Vesicles and Purinergic Signaling in Alzheimer's Disease-Joining Forces for Novel Therapeutic Approach.Brain sciences · 2025Review
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- Novel peptidomimetic compounds attenuate hypoxic-ischemic brain injury in neonatal rats.Experimental neurology · 2025Article
- Regulatory T cells in the mouse hypothalamus control immune activation and ameliorate metabolic impairments in high-calorie environments.Nature communications · 2025Article
124 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
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This paper summarizes pathological changes that affect microglial cells in the human brain during aging and in aging-related neurodegenerative diseases, primarily Alzheimer's disease (AD). It also provides examples of microglial changes that have been observed in laboratory animals during aging and in some experimentally induced lesions and disease models. Dissimilarities and similarities between humans and rodents are discussed in an attempt to generate a current understanding of microglial pathology and its significance during aging and in the pathogenesis of Alzheimer dementia (AD). The identification of dystrophic (senescent) microglia has created an ostensible conflict with prior work claiming a role for activated microglia and neuroinflammation during normal aging and in AD, and this has raised a basic question: does the brain's immune system become hyperactive (inflamed) or does it become weakened (senescent) in elderly and demented people, and what is the impact on neuronal function and cognition? Here we strive to reconcile these seemingly contradictory notions by arguing that both low-grade neuroinflammation and microglial senescence are the result of aging-associated free radical injury. Both processes are damaging for microglia as they synergistically exhaust this essential cell population to the point where the brain's immune system is effete and unable to support neuronal function.
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What OpenQuestion 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 OpenQuestion graph.