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Suggestive synergy between genetic variants in TF and HFE as risk factors for Alzheimer's disease
American journal of medical genetics. Part B, Neuropsychiatric genetics, 2010-06, Vol.153B (4), p.955-959
Kauwe, J.S.K.
Bertelsen, S.
Mayo, K.
Cruchaga, C.
Abraham, R.
Hollingworth, P.
Harold, D.
Owen, M.J.
Williams, J.
Lovestone, S.
Morris, J.C.
Goate, A.M.
2010
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Kauwe, J.S.K.
Bertelsen, S.
Mayo, K.
Cruchaga, C.
Abraham, R.
Hollingworth, P.
Harold, D.
Owen, M.J.
Williams, J.
Lovestone, S.
Morris, J.C.
Goate, A.M.
Titel
Suggestive synergy between genetic variants in TF and HFE as risk factors for Alzheimer's disease
Ist Teil von
American journal of medical genetics. Part B, Neuropsychiatric genetics, 2010-06, Vol.153B (4), p.955-959
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2010
Quelle
Wiley-Blackwell Journals
Beschreibungen/Notizen
Alzheimer's disease (AD) is a complex disease that is likely influenced by many genetic and environmental factors. Citing evidence that iron may play a role in AD pathology, Robson et al. [Robson et al. (2004); J Med Genet 41:261–265] reported that epistatic interaction between rs1049296 (P589S) in the transferrin gene (TF) and rs1800562 (C282Y) in the hemochromatosis gene (HFE) results in significant association with risk for AD. In this study we attempted to replicate their findings in a total of 1,166 cases and 1,404 controls from three European and European American populations. Allele and genotype frequencies were consistent across the three populations. Using synergy factor analysis (SFA) and Logistic Regression analysis we tested each population and the combined sample for interactions between these two SNPs and risk for AD. We observed significant association between bi‐carriers of the minor alleles of rs1049296 and rs1800562 in the combined sample using SFA (P = 0.0016, synergy factor = 2.71) and adjusted SFA adjusting for age and presence of the APOE epsilon 4 allele (P = 0.002, OR = 2.4). These results validate those of the previous report and support the hypothesis that iron transport and regulation play a role in AD pathology. © 2009 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1552-4841, 1552-485X
eISSN: 1552-485X
DOI: 10.1002/ajmg.b.31053
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2877151
Format
–
Schlagworte
Adult and adolescent clinical studies
,
Age
,
Aged
,
Alleles
,
Alzheimer Disease - epidemiology
,
Alzheimer Disease - genetics
,
Alzheimer's disease
,
Apolipoprotein E
,
Apolipoproteins E - genetics
,
Biological and medical sciences
,
Case-Control Studies
,
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
,
Environmental factors
,
Epistasis
,
Factor analysis
,
Female
,
Gene frequency
,
genetic association
,
Genotype
,
Genotypes
,
hemachromatosis gene
,
Hemochromatosis
,
Hemochromatosis - genetics
,
Humans
,
Iron
,
Iron - metabolism
,
Male
,
Medical genetics
,
Medical sciences
,
Multicenter Studies as Topic
,
Neurodegenerative diseases
,
Neurology
,
Organic mental disorders. Neuropsychology
,
Pathology
,
Polymorphism, Single Nucleotide
,
Population genetics
,
Psychology. Psychoanalysis. Psychiatry
,
Psychopathology. Psychiatry
,
Regression analysis
,
Risk
,
Risk Factors
,
Single-nucleotide polymorphism
,
Transferrin
,
Transferrin - genetics
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