ReviewCells2020
Neurovascular Inflammaging in Health and Disease.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 81 citations in OpenAlex.
- Prognostic value of the C-reactive protein to albumin ratio in patients with stroke: a meta-analysis.Scientific reports · 2025Pooled it
- Effects of Resistance Training on C-Reactive Protein and Inflammatory Cytokines in Elderly Adults: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.International journal of environmental research and public health · 2022Pooled it
- Transplantation of mesenchymal stem cells for spinal cord injury: a systematic review and network meta-analysis.Journal of translational medicine · 2021Pooled it
- APOE ɛ4 Is Associated with Postprandial Inflammation in Older Adults with Metabolic Syndrome Traits.Nutrients · 2021Trial
- Mitochondrial insufficiencies and neuroprotection in glaucoma.International ophthalmology · 2026Review
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- Remission is insufficient: predictors and mechanistic models of recurrence in late-life depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis?GeroScience · 2025Review
- Spinal Cord Injury and Ageing: The Role of Chronic Neuroinflammation.Aging and disease · 2025Review
- Gut Microbiota and Neurovascular Patterns in Amnestic Mild Cognitive Impairment.Brain sciences · 2025Article
- Perivascular glial reactivity is a feature of phosphorylated tau lesions in chronic traumatic encephalopathy.Acta neuropathologica · 2025Article
- Targeting common disease pathomechanisms to treat amyotrophic lateral sclerosis.Nature reviews. Neurology · 2025Review
- Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health.GeroScience · 2025Review
- Review
- Inflammaging and Brain Aging.International journal of molecular sciences · 2024Review
- Potential correlation between chronic periodontitis and Parkinson's disease.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024Article
- Experimental Models to Study Immune Dysfunction in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- Seasonality as a risk factor for deaths in Parkinson's disease.Clinics (Sao Paulo, Brazil) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is characterized by a chronic low-grade sterile inflammation dubbed as inflammaging, which in part originates from accumulating cellular debris. These, acting as danger signals with many intrinsic factors such as cytokines, are sensed by a network of pattern recognition receptors and other cognate receptors, leading to the activation of inflammasomes. Due to the inflammasome activity-dependent increase in the levels of pro-inflammatory interleukins (IL-1β, IL-18), inflammation is initiated, resulting in tissue injury in various organs, the brain and the spinal cord included. Similarly, in age-related diseases of the central nervous system (CNS), inflammasome activation is a prominent moment, in which cells of the neurovascular unit occupy a significant position. In this review, we discuss the inflammatory changes in normal aging and summarize the current knowledge on the role of inflammasomes and contributing mechanisms in common CNS diseases, namely Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and stroke, all of which occur more frequently with aging.
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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.