ArticleNeurobiology of aging2020
Failure to detect synergy between variants in transferrin and hemochromatosis and Alzheimer's disease in large cohort.
Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- No association of Alzheimer disease with the joint effect ofJournal of medical genetics · 2026Article
- Iron-Mediated Overexpression of Amyloid Precursor Protein via Iron Responsive mRNA in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- The Underestimated Role of Iron in Frontotemporal Dementia: A Narrative Review.International journal of molecular sciences · 2024Review
- Insights into AlphaFold's breakthrough in neurodegenerative diseases.Irish journal of medical science · 2024Review
- Article
- Iron and risk of dementia: Mendelian randomisation analysis in UK Biobank.Journal of medical genetics · 2024Article
- HFE Mutations in Neurodegenerative Disease as a Model of Hormesis.International journal of molecular sciences · 2024Review
- Imbalance of Essential Metals in Traumatic Brain Injury and Its Possible Link with Disorders of Consciousness.International journal of molecular sciences · 2023Review
- Hemochromatosis Mutations, Brain Iron Imaging, and Dementia in the UK Biobank Cohort.Journal of Alzheimer's disease : JAD · 2021Article
- Evaluation of serum iron overload, AST:ALT ratio and logBMC research notes · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia and, despite decades of effort, there is no effective treatment. In the last decade, many association studies have identified genetic markers that are associated with AD status. Two of these studies suggest that an epistatic interaction between variants rs1049296 in the transferrin (TF) gene and rs1800562 in the homeostatic iron regulator (HFE) gene, commonly known as hemochromatosis, is in genetic association with AD. TF and HFE are involved in the transport and regulation of iron in the brain, and disrupting these processes exacerbates AD pathology through increased neurodegeneration and oxidative stress. However, by using a significantly larger data set from the Alzheimer's Disease Genetics Consortium, we fail to detect an association between TF rs1049296 or HFE rs1800562 with AD risk (TF rs1049296 p = 0.38 and HFE rs1800562 p = 0.40). In addition, logistic regression with an interaction term and a synergy factor analysis both failed to detect epistasis between TF rs1049296 and HFE rs1800562 (SF = 0.94; p = 0.48) in AD cases. Each of these analyses had sufficient statistical power (power > 0.99), suggesting that previously reported associations may be the result of more complex epistatic interactions, genetic heterogeneity, or false-positive associations because of limited sample sizes.
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Registered trials
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