ReviewClinical & experimental neuroimmunology2018
Neuroinflammation in mouse models of Alzheimer's disease.
Review in Clinical & experimental neuroimmunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 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
67 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Macrophage mechanobiology: from sensing to disease.Frontiers in immunology · 2026Pooled it
- Experimental procedures for flow cytometry of wild-type mouse brain: a systematic review.Frontiers in immunology · 2023Pooled it
- Expression of GPR34 in microglia remains stable in human Alzheimer's disease.Acta neuropathologica · 2026Article
- Chronic central-targeted Interleukin-6 overexpression promotes hippocampal and cortical neuropathology in the Tg2576 mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Restriction of Individual Branched-Chain Amino Acids has Distinct Effects on the Development and Progression of Alzheimer's Disease in 3xTg Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Navigation Between Alzheimer's Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology-Genetics and Neuroinflammation.International journal of molecular sciences · 2025Review
- Article
- Gene Expression Signatures of Immaturity, Decreased pH, and Neural Hyperexcitation in the Hippocampus of Alzheimer's Disease Model Mice.Neuropsychopharmacology reports · 2025Article
- Early and progressive retinal microglial changes in APPFrontiers in aging neuroscience · 2025Article
- Air Pollution as an Environmental Risk Factor for Alzheimer's Disease and Related Dementias.Medical research archives · 2024Article
- Physical Exercise Counteracts Aging-Associated White Matter Demyelination Causing Cognitive Decline.Aging and disease · 2024Review
- Age-Related Retinal Layer Thickness Changes Measured by OCT inInternational journal of molecular sciences · 2024Article
- Retinal Vascular and Structural Changes in the Murine Alzheimer'sBiomolecules · 2024Article
- FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024Article
- From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Rodent Models of Alzheimer's Disease: Past Misconceptions and Future Prospects.International journal of molecular sciences · 2024Review
- Experimental colitis in young Tg2576 mice accelerates the onset of an Alzheimer's-like clinical phenotype.Alzheimer's research & therapy · 2024Article
- Switch of innate to adaptative immune responses in the brain of patients with Alzheimer's disease correlates with tauopathy progression.npj aging · 2024Article
- OCT Imaging in Murine Models of Alzheimer's Disease in a Systematic Review: Findings, Methodology and Future Perspectives.Biomedicines · 2024Review
7 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common type of neurocognitive disorder. Although both amyloid β peptide deposition and neurofibrillary tangle formation in the AD brain have been established as pathological hallmarks of the disease, many other factors contribute in a complex manner to the pathogenesis of AD before clinical symptoms of the disease become apparent. Longitudinal pathophysiological processes cause patients' brains to exist in a state of chronic neuroinflammation, with glial cells acting as key regulators of the neuroinflammatory state. However, the detailed molecular and cellular mechanisms of glial function underlying AD pathogenesis remain elusive. Furthermore, recent studies have shown that peripheral inflammatory conditions affect glial cells in the brain through a process of neuroimmune communication. Such disease complexities make it difficult for the pathogenesis of AD to be understood, and impede the development of effective therapeutic strategies to combat the disease. Relevant AD animal models are thus likely to serve as a key resource to overcome many of these issues. Furthermore, as the pathogenesis of AD might be linked to conditions both within the brain as well as peripherally, it might become necessary for AD to be studied as a whole-body disorder. The present review aimed to summarize insights regarding current AD research, and share perspectives for understanding glial function in the context of the pathogenesis of AD.
Indexed as
Identifiers
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.