ArticlePloS one2012
Involvement of receptor tyrosine kinase Tyro3 in amyloidogenic APP processing and β-amyloid deposition in Alzheimer's disease models.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- lncRNAs: key player in Aβ deposition.RNA biology · 2026Review
- Selective Inactivation of Astrocytic Monoacylglycerol Lipase for Alzheimer's Disease Therapy.bioRxiv : the preprint server for biology · 2025Article
- Different inflammatory signatures based on CSF biomarkers relate to preserved or diminished brain structure and cognition.Molecular psychiatry · 2024Observational
- Prognostic DNA mutation and mRNA expression analysis of perineural invasion in oral squamous cell carcinoma.Scientific reports · 2024Article
- Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022Review
- Intermittent hypoxia treatment alleviates memory impairment in the 6-month-old APPswe/PS1dE9 mice and reduces amyloid beta accumulation and inflammation in the brain.Alzheimer's research & therapy · 2021Article
- Molecular Mechanism of Vitamin K2 Protection against Amyloid-β-Induced Cytotoxicity.Biomolecules · 2021Article
- TAM Signaling in the Nervous System.Brain plasticity (Amsterdam, Netherlands) · 2021Article
- Vitamin K Concentration and Cognitive Status in Elderly Patients on Anticoagulant Therapy: A Pilot Study.Journal of aging research · 2020Article
- Dysregulation of TLR5 and TAM Ligands in the Alzheimer's Brain as Contributors to Disease Progression.Molecular neurobiology · 2019Article
- The Relationships Between Vitamin K and Cognition: A Review of Current Evidence.Frontiers in neurology · 2019Review
- TAM Receptor Pathways at the Crossroads of Neuroinflammation and Neurodegeneration.Disease markers · 2019Review
- Sulforaphane rescues amyloid-β peptide-mediated decrease in MerTK expression through its anti-inflammatory effect in human THP-1 macrophages.Journal of neuroinflammation · 2018Article
- Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology.Nature communications · 2018Article
- SQYZ granules, a traditional Chinese herbal, attenuate cognitive deficits in AD transgenic mice by modulating on multiple pathogenesis processes.American journal of translational research · 2018Article
- Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking.Essays in biochemistry · 2017Review
- IDENTIFICATION OF DISCRIMINATIVE IMAGING PROTEOMICS ASSOCIATIONS IN ALZHEIMER'S DISEASE VIA A NOVEL SPARSE CORRELATION MODEL.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2017Article
- Altered Expression Patterns of Inflammation-Associated and Trophic Molecules in Substantia Nigra and Striatum Brain Samples from Parkinson's Disease, Incidental Lewy Body Disease and Normal Control Cases.Frontiers in neuroscience · 2015Article
- Alteration of Golgi Structure by Stress: A Link to Neurodegeneration?Frontiers in neuroscience · 2015Article
- Triptolide treatment reduces Alzheimer's disease (AD)-like pathology through inhibition of BACE1 in a transgenic mouse model of AD.Disease models & mechanisms · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease known to humankind. It is characterized by brain atrophy, extracellular amyloid plaques, and intracellular neurofibril tangles. β-Amyloid cascade is considered the major causative player in AD. Up until now, the mechanisms underlying the process of Aβ generation and accumulation in the brain have not been well understood. Tyro3 receptor belongs to the TAM receptor subfamily of receptor protein tyrosine kinases (RPTKs). It is specifically expressed in the neurons of the neocortex and hippocampus. In this study, we established a cell model stably expressing APPswe mutants and producing Aβ. We found that overexpression of Tyro3 receptor in the cell model significantly decreased Aβ generation and also down-regulated the expression of β-site amyloid precursor protein cleaving enzyme (BACE1). However, the effects of Tyro3 were inhibited by its natural ligand, Gas6, in a concentration-dependent manner. In order to confirm the role of Tyro3 in the progression of AD development, we generated an AD transgenic mouse model accompanied by Tyro3 knockdown. We observed a significant increase in the number of amyloid plaques in the hippocampus in the mouse model. More plaque-associated clusters of astroglia were also detected. The present study may help researchers determine the role of Tyro3 receptor in the neuropathology of AD.
Indexed as
Identifiers
What OpenQuestion holds
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.