ReviewMolecular neurodegeneration2022
Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2.
Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
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Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Gene expression meta-analysis in the prefrontal cortex: unraveling biological underpinnings of suicidal risk.BMC psychiatry · 2026Pooled it
- Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Article
- Personalized single-cell transcriptomics reveals molecular diversity in Alzheimer's disease.Nature communications · 2026Article
- High-resolution CRISPR/Cas9 screens identify PAK2 as a suppressor of macrophage proliferation.bioRxiv : the preprint server for biology · 2026Article
- Article
- TREM2-Targeting peptide tracer for neuroinflammation PET imaging.European journal of nuclear medicine and molecular imaging · 2026Article
- Multi-omics identification of haptoglobin as a novel target for increased Alzheimer's disease risk associated with obesity through inhibiting the phagocytosis of Aβ by disease-associated microglia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- CD33 and clusterin interact biophysically and genetically to modulate Alzheimer risk.Nature communications · 2026Article
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- Genome-wide pleiotropic analysis identifies shared genetic architecture within the cognition-immune nexus.Translational psychiatry · 2026Article
- In Silico Drug Repositioning Identifies SYK Kinase Inhibitors as Potential Neuroprotective Agents for Ataxia-Telangiectasia.Chemical biology & drug design · 2026Article
- Neuroinflammation and Tauopathies.Molecular biology reports · 2026Review
- Clustering Single-Cell RNA-Seq Data with Low-Rank Matrix Factorization and Local Graph Regularization.Interdisciplinary sciences, computational life sciences · 2026Article
- The impact of Trem2-mediated macrophage polarization on the mechanisms of allergic rhinitis.Scientific reports · 2026Article
- The role of DAP12 in immune-related inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Native PLGA nanoparticles attenuate disease pathology via multiple pathways in 5xFAD Alzheimer's model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Alignment of spatial transcriptomics slices across diseases, platforms and conditions.Genome medicine · 2026Article
- Genome-wide consensus transcriptional signatures identify synaptic pruning linking Alzheimer's disease and epilepsy.Molecular psychiatry · 2026Article
- Impaired TGFβ Signaling in Plaque-Associated Microglia.Biomolecules · 2026Article
50 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 1 country.
Funding
Abstract
TYROBP (also known as DAP12 or KARAP) is a transmembrane adaptor protein initially described as a receptor-activating subunit component of natural killer (NK) cells. TYROBP is expressed in numerous cell types, including peripheral blood monocytes, macrophages, dendritic cells, and osteoclasts, but a key point of recent interest is related to the critical role played by TYROBP in the function of many receptors expressed on the plasma membrane of microglia. TYROBP is the downstream adaptor and putative signaling partner for several receptors implicated in Alzheimer's disease (AD), including SIRP1β, CD33, CR3, and TREM2. TYROBP has received much of its current notoriety because of its importance in brain homeostasis by signal transduction across those receptors. In this review, we provide an overview of evidence indicating that the biology of TYROBP extends beyond its interaction with these four ligand-binding ectodomain-intramembranous domain molecules. In addition to reviewing the structure and localization of TYROBP, we discuss our recent progress using mouse models of either cerebral amyloidosis or tauopathy that were engineered to be TYROBP-deficient or TYROBP-overexpressing. Remarkably, constitutively TYROBP-deficient mice provided a model of genetic resilience to either of the defining proteinopathies of AD. Learning behavior and synaptic electrophysiological function were preserved at normal physiological levels even in the face of robust cerebral amyloidosis (in APP/PSEN1;Tyrobp
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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.