ArticleNeurobiology of aging2017
Regulatory region genetic variation is associated with FYN expression in Alzheimer's disease.
Article in Neurobiology of aging, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Fyn kinase: a key mechanistic regulator and therapeutic target in tauopathy and neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Fyn-dependent Tau microcluster formation seeds and boosts extensive Tau pathology.Acta neuropathologica · 2025Article
- FYN Tyrosine Kinase Gene Polymorphisms in Alcohol-Dependent Korean Patients.Alpha psychiatry · 2025Article
- Loss of miR-369 Promotes Tau Phosphorylation by Targeting the Fyn and Serine/Threonine-Protein Kinase 2 Signaling Pathways in Alzheimer's Disease Mice.Frontiers in aging neuroscience · 2019Article
- Targeting Fyn Kinase in Alzheimer's Disease.Biological psychiatry · 2018Review
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Neurofibrillary tangles (NFTs), composed of hyperphosphorylated tau, are a key pathologic feature of Alzheimer's disease (AD). Tau phosphorylation is under the control of multiple kinases and phosphatases, including Fyn. Previously, our group found an association between 2 regulatory single nucleotide polymorphisms in the FYN gene with increased tau levels in the cerebrospinal fluid. In this study, we hypothesized that Fyn expression in the brain is influenced by AD status and genetic content. We found that Fyn protein, but not messenger RNA, levels were increased in AD patients compared to cognitively normal controls and are associated with regulatory region single nucleotide polymorphisms. In addition, the expression of the FYN 3'UTR can decrease expression in multiple cell lines, suggesting this regulatory region plays an important role in FYN expression. Taken together, these data suggest that FYN expression is regulated according to AD status and regulatory region haplotype, and genetic variants may be instrumental in the development of neurofibrillary tangles in AD and other tauopathies.
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Registered trials
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