ArticleMolecular neurobiology2019
Dysregulation of TLR5 and TAM Ligands in the Alzheimer's Brain as Contributors to Disease Progression.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
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- The Peripheral Amyloid-β Nexus: Connecting Alzheimer's Disease with Atherosclerosis through Shared Pathophysiological Mechanisms.Neuromolecular medicine · 2025Review
- A Mouse Model of Sporadic Alzheimer's Disease with Elements of Major Depression.Molecular neurobiology · 2025Article
- Long Non-Coding RNAs and Alzheimer's Disease: Towards Personalized Diagnosis.International journal of molecular sciences · 2024Article
- Different inflammatory signatures based on CSF biomarkers relate to preserved or diminished brain structure and cognition.Molecular psychiatry · 2024Observational
- Neuroinflammation in Alzheimer's Disease: A Potential Role of Nose-Picking in Pathogen Entry via the Olfactory System?Biomolecules · 2023Review
- Gas6/AXL pathway: immunological landscape and therapeutic potential.Frontiers in oncology · 2023Review
- Revisiting the neuroinflammation hypothesis in Alzheimer's disease: a focus on the druggability of current targets.Frontiers in pharmacology · 2023Review
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- Toll-like receptor-mediated neuroinflammation: relevance for cognitive dysfunctions.Trends in pharmacological sciences · 2022Review
- Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration.Cell death & disease · 2022Review
- Profiling Microglia in a Mouse Model of Machado-Joseph Disease.Biomedicines · 2022Article
- The Innate and Adaptive Immune Cells in Alzheimer's and Parkinson's Diseases.Oxidative medicine and cellular longevity · 2022Review
- Wuzi-Yanzong prescription alleviates spermatogenesis disorder induced by heat stress dependent on Akt, NF-κB signaling pathway.Scientific reports · 2021Article
- Delivery of toll-like receptor agonists by complement C3-targeted liposomes activates immune cells and reduces tumour growth.Journal of drug targeting · 2021Article
- Computational Interspecies Translation Between Alzheimer's Disease Mouse Models and Human Subjects Identifies Innate Immune Complement, TYROBP, and TAM Receptor Agonist Signatures, Distinct From Influences of Aging.Frontiers in neuroscience · 2021Article
- TAM Signaling in the Nervous System.Brain plasticity (Amsterdam, Netherlands) · 2021Article
- Activation of Toll-like receptor 5 in microglia modulates their function and triggers neuronal injury.Acta neuropathologica communications · 2020Article
- Gas6 Inhibits Toll-Like Receptor-Mediated Inflammatory Pathways in Mouse MicrogliaFrontiers in cellular neuroscience · 2020Article
- TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration.Disease markers · 2019Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The hypothesis that accumulation of beta-amyloid (Aβ) species in the brain represents a major event in Alzheimer's disease (AD) pathogenesis still prevails; nevertheless, an array of additional pathological processes contributes to clinical presentation and disease progression. We sought to identify novel targets for AD within genes related to amyloid precursor protein (APP) processing, innate immune responses, and the catecholamine system. Through a series of bioinformatics analyses, we identified TLR5 and other genes involved in toll-like receptor (TLR) signaling as potential AD targets. It is believed that Aβ species induce activation of microglia and astrocytes in AD, with a negative impact on disease progression. The TAM (Tyro3, Axl, Mer) family of receptor tyrosine kinases plays pivotal roles in limiting inflammatory responses upon TLR stimulation, for which we further studied their implication in the TLR5 alterations observed in AD. We validated the up-regulation of TLR5 in the frontal cortex of moderate AD cases. In addition, we observed up-regulation of the TAM ligands protein S (PROS1), galectin-3 (LGALS3), and Tulp-1. Furthermore, we identified an association of the TAM ligand GAS6 with AD progression. In THP-1 cells, co-stimulation with Aβ and flagellin for 24 h induced up-regulation of TYRO3 and GAS6, which could be prevented by neutralization of TLR5. Our results underscore the role of TLR dysregulations in AD, suggesting the presence of an immunosuppressive response during moderate disease stages, and implicate TAM signaling in AD immune dysregulation.
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