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Failure to detect synergy between variants in transferrin and hemochromatosis and Alzheimer's disease in large cohort.

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.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Vance E,Gonzalez Murcia JD,Miller JB,Alzheimer's Disease Genetics Consortium (ADGC).,Staley L,Crane PK,Mukherjee S,Kauwe JSK

doi

10.1016/j.neurobiolaging.2020.01.013

subject

Has Abstract

pub_date

2020-05-01 00:00:00

pages

142.e9-142.e12

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(20)30027-0

journal_volume

89

pub_type

杂志文章

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