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A risk for early-onset Alzheimer's disease associated with the APBB1 gene (FE65) intron 13 polymorphism.

Authors: Cousin, E  Hannequin, D  Ricard, S  Mace, S  Genin, E  Chansac, C  Brice, A  Dubois, B  Frebourg, T  Mercken, L  Benavides, J  Pradier, L  Campion, D  Deleuze, JF 
Citation: Cousin E, etal., Neurosci Lett. 2003 May 15;342(1-2):5-8.
Pubmed: (View Article at PubMed) PMID:12727304

Alzheimer's disease (AD) is a genetically complex neurodegenerative disorder and the leading cause of dementia of the elderly. Recently, Hu et al. suggested that a trinucleotide deletion in intron 13 of the APBB1 gene was a factor protecting against late-onset AD. We report here the results of a case/control study aimed at replicating this association. Our study included 461 AD patients and 397 matched controls. We compared the allele and genotype frequencies of the polymorphism between the two groups but did not find any statistically significant difference (P=0.08 and P=0.09, respectively). By contrast, adjusting for age and sex, we found a slight risk associated with the deletion (odds ratio=1.47, 95% confidence interval=1.05-2.04). Stratification by age showed that the risk effect associated with the deletion concerned subjects aged less than 65 years.


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CRRD Object Information
CRRD ID: 10054031
Created: 2015-07-22
Species: All species
Last Modified: 2015-07-22
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.