Article

No association between the insulin degrading enzyme gene and Alzheimer's disease in a Japanese population.

Kasaoka Hospital, Kasaoka, Japan.
American Journal of Medical Genetics Part B Neuropsychiatric Genetics (impact factor: 3.7). 03/2004; 125B(1):87-91. DOI:10.1002/ajmg.b.20106 pp.87-91
Source: PubMed

ABSTRACT Susceptibility to Alzheimer's disease (AD) is thought to be regulated by multiple genetic factors. Recently, three independent studies have reported that loci on chromosome 10q are linked with AD, and the insulin degrading enzyme (IDE; MIM 146680) gene located on chromosome 10q23-q25; IDE is located close to the maker D10S583, which exhibits a maximum LOD score for late-onset AD. We examined seven polymorphisms in the IDE gene, the marker D10S583 in the 5' flanking region, and SNPs in introns 1, 3, 11, 20, 21, and 22 (rs#1999764, 1855915, 1970244, 538469, 551266, and 489517, respectively). Four SNPs in introns 3, 11, 20, and 22 did not exhibit any polymorphisms in the Japanese population that was studied. D10S583 and two SNPs in introns 1 and 21 did not exhibit a significant association with early- or late-onset AD. In addition, no associations were observed for subgroups of AD grouped according to APOE status. The present study indicates that the IDE gene polymorphisms do not confer susceptibility to early- or late-onset AD at least in a Japanese population.

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    Article: Weak independent association signals between IDE polymorphisms, Alzheimer's disease and cognitive measures.
    Jakob C Mueller, Matthias Riemenschneider, Andreas Schoepfer-Wendels, Henning Gohlke, Lidija Konta, Patricia Friedrich, Thomas Illig, Simon M Laws, Hans Förstl, Alexander Kurz
    [show abstract] [hide abstract]
    ABSTRACT: Functional and genetic studies suggest that insulin-degrading enzyme (IDE) may be a strong functional and positional candidate. As there is a lack of consensus in regards to the level and location of IDE association signals we aimed to clarify these discrepancies through genotyping 28 SNPs in a large case-control collective together with quantitative measures of cognitive ability (MMSE). Four SNPs (rs11187007, rs2149632_ide12, rs11187033, rs11187040) were found to be associated with AD (nominal p<0.01). Tests with MMSE scores adjusted for disease duration identified associations, with the most significant result for rs1999763 (nominal p=0.008). Similarly, different reconstructed IDE haplotypes were associated with AD and higher MMSE scores. The association signals are only borderline significant after adjustment for multiple testing, but add further evidence to previous published results on the association between IDE and AD or MMSE. A subgroup analysis indicated more prominent associations with AD in younger, and with MMSE in older patients. There may be two independent effects mediated by IDE variants, risk for AD and modification of disease progression.
    Neurobiology of aging 05/2007; 28(5):727-34. · 5.94 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

5' flanking region
 
Alzheimer's disease
 
APOE status
 
chromosome 10q
 
early-
 
IDE
 
IDE gene
 
IDE gene polymorphisms
 
independent studies
 
insulin degrading enzyme
 
introns 3
 
late-onset AD
 
maximum LOD score
 
multiple genetic factors
 
significant association
 
SNPs
 
Susceptibility
 

Ayumu Sakai