ReviewNeuropathology and applied neurobiology2013
Review: experimental manipulations of microglia in mouse models of Alzheimer's pathology: activation reduces amyloid but hastens tau pathology.
Review in Neuropathology and applied neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Microglial Drivers of Alzheimer's Disease Pathology: An Evolution of Diverse Participating States.Proteins · 2025Review
- Interplay of Neuroinflammation and Gut Microbiota Dysbiosis in Alzheimer's Disease Using Diffusion Kurtosis Imaging Biomarker in 3 × Tg-AD Mouse Models.ACS chemical neuroscience · 2025Article
- Article
- Lactobacillus-derived extracellular vesicles counteract Aβ42-induced abnormal transcriptional changes through the upregulation of MeCP2 and Sirt1 and improve Aβ pathology in Tg-APP/PS1 mice.Experimental & molecular medicine · 2023Article
- Influence of Host Age on Intracranial AAV9 TauP301L Induced Tauopathy.Journal of Alzheimer's disease : JAD · 2023Article
- Diversity of transcriptomic microglial phenotypes in aging and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Review
- Microglia-Mediated Inflammation and Neural Stem Cell Differentiation in Alzheimer's Disease: Possible Therapeutic Role of KFrontiers in cellular neuroscience · 2022Review
- Knowledge gaps in Alzheimer's disease immune biomarker research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Review
- Innate immunity stimulation via CpG oligodeoxynucleotides ameliorates Alzheimer's disease pathology in aged squirrel monkeys.Brain : a journal of neurology · 2021Article
- Microglia is associated with p-Tau aggregates in the olfactory bulb of patients with neurodegenerative diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Oxiracetam Offers Neuroprotection by Reducing Amyloid β-Induced Microglial Activation and Inflammation in Alzheimer's Disease.Frontiers in neurology · 2020Article
- Alzheimer's Disease: What Can We Learn From the Peripheral Olfactory System?Frontiers in neuroscience · 2020Review
- TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration.Disease markers · 2019Review
- Chronic PD-1 Checkpoint Blockade Does Not Affect Cognition or Promote Tau Clearance in a Tauopathy Mouse Model.Frontiers in aging neuroscience · 2019Article
- The small molecule CA140 inhibits the neuroinflammatory response in wild-type mice and a mouse model of AD.Journal of neuroinflammation · 2018Article
- Microglia in Alzheimer's disease.The Journal of clinical investigation · 2017Review
- Innate Immunity Stimulation via Toll-Like Receptor 9 Ameliorates Vascular Amyloid Pathology in Tg-SwDI Mice with Associated Cognitive Benefits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Involvement of the Bradykinin BFrontiers in endocrinology · 2017Article
- Identifying biomarkers of dementia prevalent among amnestic mild cognitively impaired ethnic female patients.Alzheimer's research & therapy · 2016Article
- The roles of inflammation and immune mechanisms in Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The inflammation hypothesis of Alzheimer's pathogenesis has directed much scientific effort towards ameliorating this disease. The development of mouse models of amyloid deposition permitted direct tests of the proposal that amyloid-activated microglia could cause neurodegeneration in vivo. Many approaches to manipulating microglial activation have been applied to these mouse models, and are the subject of this review. In general, these results do not support a direct neuricidal action of microglia in mouse amyloid models under any activation state. Some of the manipulations cause both a reduction in pathology and a reduction in microglial activation. However, at least for agents like ibuprofen, this outcome may result from a direct action on amyloid production, and a reduction in the microglial-provoking amyloid deposits, rather than from reduced microglial activation leading to a decline in amyloid deposition. Instead, a surprising number of the experimental manipulations which increase microglial activation lead to enhanced clearance of the amyloid deposits. Both the literature and new data presented here suggest that either classical or alternative activation of microglia can lead to enhanced amyloid clearance. However, a limited number of studies comparing the same treatments in amyloid-depositing vs. tau-depositing mice find the opposite effects. Treatments that benefit amyloid pathology accelerate tau pathology. This observation argues strongly that potential treatments be tested for impact on both amyloid and tau pathology before consideration of testing in humans.
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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.