TYROBP in Alzheimer’s Disease
Abstract
Recently, studies have provided convincing data that TYRO protein tyrosine kinase-binding protein (TYROBP), a key regulator in immune systems, is significantly upregulated in the brain of patients with Alzheimer's disease (AD). TYROBP acts as a signaling adaptor protein for numerous cell surface receptors, playing important roles in signal transduction in dendritic cells, osteoclasts, macrophages, and microglia. Although several TYROBP-related cell surface receptors including triggering receptor expressed on myeloid 2 (TREM2), signal regulatory protein β1 (SIRPβ1), and complement receptor 3 (CR3) were found to participate in the pathogenesis of AD, the role of TYROBP in AD still remains elusive. Emerging piece of evidence has demonstrated that TYROBP could enhance phagocytic activity of microglia, which is responsible for the clearance of amyloid-β (Aβ) peptides and apoptotic neurons. TYROBP also participates in suppression of inflammatory responses by repression of microglia-mediated cytokine production and secretion. In this article, we introduce the structure, localization, and function of TYROBP. Meanwhile, we review recent articles concerning the association of TYROBP and its related receptors with AD pathogenesis and speculate the possible roles of TYROBP in this disease. Based on the potential protective actions of TYROBP in AD pathogenesis, targeting TYROBP might provide new opportunities for AD treatment.
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TYROBP is a key regulator of the complement pathway in the immune/microglia network, which is activated as Aβ accumulates in LOAD brains.
“TYROBP (TYRO protein tyrosine kinase-binding protein) is a key regulator of the complement pathway in the immune/microglia network, which is activated as Aβ accumulates in LOAD brains [56, 90].”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [90]
Recent studies suggested TYROBP-mediated signaling is involved in multiple important functions as aggregating Aβ activates microglia, including enhanced phagocytosis of damaged neurons and suppression of inflammatory responses, as well as neuronal pruning activity.
“Recent studies suggested TYROBP-mediated signaling is involved in multiple important functions as aggregating Aβ activates microglia, including enhanced phagocytosis of damaged neurons [56, 90] and suppression of inflammatory responses [94], as well as neuronal pruning activity [56].”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [90]
TYROBP is a transmembrane adaptor protein for TREM2, SIRPβ1, and CR3 receptors, which are known to be involved in AD pathogenesis.
“TYROBP is a transmembrane adaptor protein for TREM2, SIRPβ1, and CR3 receptors, which are known to be involved in AD pathogenesis [90–92].”
From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [90]
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References 59 · Cited by 113
- Authors
- Ma, J., Jiang, T., Tan, L., & Yu, J.-T.
- Affiliations
- Qingdao University (CN)
- Qingdao Municipal Hospital (CN)
- Corresponding author
- Tan, Lan
- Yu, Jin-Tai
- Venue
- Molecular Neurobiology
- Published
- 2014-07-23
- Volume
- 51
- Issue
- 2
- Pages
- 820-826
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W2162070793
- Cited by
- 113
- References
- 59
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 14 · 2023: 8 · 2022: 21 · 2021: 12 · 2020: 12 · 2019: 8 · 2018: 9 · 2017: 3 · 2016: 9 · 2015: 3
- FWCI
- 0.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- TYROBP, Alzheimer's disease, microglia, TREM2, complement receptor 3, phagocytosis, amyloid-beta clearance, neuroinflammation, cytokine production, adaptor proteins, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Membrane Proteins, Signal Transduction, Microglia, Adaptor Proteins, Signal Transducing
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