Microglial TYROBP/DAP12 in Alzheimer's Disease: Transduction of Physiological and Pathological Signals Across TREM2
Open accessAbstract
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 −/− mice) or tauopathy (in MAPT P301S ; Tyrobp −/− mice). A fundamental underpinning of the functional synaptic dysfunction associated with each proteotype was an accumulation of complement C1q. TYROBP deficiency prevented C1q accumulation associated with either proteinopathy. Based on these data, we speculate that TYROBP plays a key role in the microglial sensome and the emergence of the disease-associated microglia (DAM) phenotype. TYROBP may also play a key role in the loss of markers of synaptic integrity (e.g., synaptophysin-like immunoreactivity) that has long been held to be the feature of human AD molecular neuropathology that most closely correlates with concurrent clinical cognitive function.
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PU.1 induces the transcription of several surface receptors, such as ITGAM, VCAM1, TREM2, and TYROBP, thereby enhancing microglial phagocytic capacity for Aβ clearance.
“As shown in Figure 1, previous studies showed that PU.1 induces the transcription of several surface receptors, such as Integrin subunit alpha M (ITGAM, also known as CD11b), vascular cell adhesion molecule 1 (VCAM1, also known as CD106), TREM2, and TYROBP [32, 55], thereby enhancing microglial phagocytic capacity for Aβ clearance [56, 57].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [56]
The section “TYROBP: A hub for phagocytosis signaling pathways?” links TYROBP and CD11b/ITGAM to microglial phagocytosis and amyloid clearance or compaction. The section “TYROBP, sensome, and microglial switching” also associates TREM2 with a phagocytosis-related microglial state. These passages do not establish that PU.1 induces transcription of the listed genes, include VCAM1 in that mechanism, or show that PU.1 thereby enhances Aβ clearance; no page numbers were available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTYROBP is a key regulator of this gene-network module, driving the expression of other genes.
“TYROBP is a key regulator of this gene-network module, driving the expression of other genes.”
From The effect of Abi3 locus deletion on the progression of Alzheimer’s disease-related pathologies (2023) · cites this paper as [48]
The Background and “TYROBP in Alzheimer’s disease” sections describe TYROBP as a key network hub and driver in sporadic late-onset Alzheimer’s disease. The “TYROBP: A hub for phagocytosis signaling pathways?” section reports altered Itgam expression when TYROBP is deleted, but the copy does not establish that TYROBP drives expression of other genes across the specified network module. The indexed passages provide section labels but no page numbers. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTYROBP is the downstream signaling mediator of several microglial receptors implicated in AD, such as TREM2 and CD33.
“Interestingly, it is also the downstream signaling mediator of several microglial receptors that are implicated in AD, such as TREM2 and CD33 (41, 48).”
From The effect of Abi3 locus deletion on the progression of Alzheimer’s disease-related pathologies (2023) · cites this paper as [48]
The Abstract identifies TYROBP as a downstream adaptor and putative signaling partner for AD-implicated receptors including TREM2 and CD33. The “TYROBP receptors in the brain” section supports signaling through TYROBP for TREM2, but says only that mouse CD33 is suggested to signal through it; human CD33 instead has ITIM motifs and associates with SHP-1. The claim omits that qualification for CD33. (LLM, conf=0.88)
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- Authors
- Haure-Mirande, J.-V., Audrain, M., Ehrlich, M. E., & Gandy, S.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- James J. Peters VA Medical Center (US)
- Corresponding author
- Ehrlich, Michelle E.
- Gandy, Sam
- Venue
- Molecular Neurodegeneration
- Published
- 2022-08-24
- Volume
- 17
- Issue
- 1
- Pages
- 55-55
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC9404585
- OpenAlex
- W4292939095
- Cited by
- 159
- References
- 142
- Citations by year
- 2026: 41 · 2025: 41 · 2024: 47 · 2023: 28 · 2022: 2
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (U01AG046170, R01AG057907, R03AG070710)
- Cure Alzheimer's Fund
- BrightFocus Foundation (A2018253F, A2016482F)
- Mount Sinai Alzheimer’s Disease Research Center (AG005138, P30AG066514)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- TYROBP, DAP12, Alzheimer's disease, microglia, TREM2, C1q, cerebral amyloidosis, tauopathy, disease-associated microglia, synaptic dysfunction, synaptophysin, receptor signaling
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Membrane Glycoproteins, Membrane Proteins, Receptors, Immunologic, Microglia, Tauopathies, Adaptor Proteins, Signal Transducing, Mice
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