ArticleActa neuropathologica2017
Deficiency of TYROBP, an adapter protein for TREM2 and CR3 receptors, is neuroprotective in a mouse model of early Alzheimer's pathology.
Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.
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Who cites it
78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 126 citations in OpenAlex.
- Transcriptomics Meta-Analysis Reveals Phagosome and Innate Immune System Dysfunction as Potential Mechanisms in the Cortex of Alzheimer's Disease Mouse Strains.Journal of molecular neuroscience : MN · 2023Pooled it
- The landscape of multiscale transcriptomic networks and key regulators in Parkinson's disease.Nature communications · 2019Pooled it
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- Single-cell transcriptomic analysis reveals APOE genotype-dependent sex differences in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Genome-wide consensus transcriptional signatures identify synaptic pruning linking Alzheimer's disease and epilepsy.Molecular psychiatry · 2026Article
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- DAP12 deletion reduces neuronal SLIT2 and demyelination and enhances brain resilience in female tauopathy mice.Molecular neurodegeneration · 2025Article
- Human amyotrophic lateral sclerosis/motor neuron disease: The disease-associated microglial pathway is upregulated while APOE genotype governs risk and survival.Brain pathology (Zurich, Switzerland) · 2025Article
- Microglial CLEC7A restrains amyloid beta plaque pathology in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- TREM2-Mediated Myeloid Cells Protect Against Pathological Choroidal Neovascularization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Connexin43 hemichannel blockade turns microglia neuroprotective and mitigates cognitive deficits in a mouse model of amyloidosis.Nature communications · 2025Article
- Monoallelic TYROBP deletion is a novel risk factor for Alzheimer's disease.Molecular neurodegeneration · 2025Article
- Myeloid lineage C3 induces reactive gliosis and neuronal stress during CNS inflammation.Nature communications · 2025Article
- Validation of the Mechanism of Action of TYROBP Related to Blood-Brain Barrier Function in Intracerebral Hemorrhage by Bioinformatics Analysis.Iranian journal of biotechnology · 2025Article
- Differential Expression of Neurodegeneration-Related Genes in SH-SY5Y Neuroblastoma Cells Under the Influence of Cyclophilin A: Could the Enzyme be a Likely Trigger and Therapeutic Target for Alzheimer's Disease?Neurochemical research · 2024Article
- The Mechanistic Link Between Tau-Driven Proteotoxic Stress and Cellular Senescence in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Connecting dementia risk loci to the CSF proteome identifies pathophysiological leads for dementia.Brain : a journal of neurology · 2024Article
- TYROBP serve as potential immune-related signature genes in the acute phase of intracerebral hemorrhage.Scientific reports · 2024Article
- TREM2-dependent activation of microglial cell protects photoreceptor cell during retinal degeneration via PPARγ and CD36.Cell death & disease · 2024Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Conventional genetic approaches and computational strategies have converged on immune-inflammatory pathways as key events in the pathogenesis of late onset sporadic Alzheimer's disease (LOAD). Mutations and/or differential expression of microglial specific receptors such as TREM2, CD33, and CR3 have been associated with strong increased risk for developing Alzheimer's disease (AD). DAP12 (DNAX-activating protein 12)/TYROBP, a molecule localized to microglia, is a direct partner/adapter for TREM2, CD33, and CR3. We and others have previously shown that TYROBP expression is increased in AD patients and in mouse models. Moreover, missense mutations in the coding region of TYROBP have recently been identified in some AD patients. These lines of evidence, along with computational analysis of LOAD brain gene expression, point to DAP12/TYROBP as a potential hub or driver protein in the pathogenesis of AD. Using a comprehensive panel of biochemical, physiological, behavioral, and transcriptomic assays, we evaluated in a mouse model the role of TYROBP in early stage AD. We crossed an Alzheimer's model mutant APP
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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 Socratic graph.