Wragg et al.[1996: Lancet 347:509-512] recorded an association between the intron-based presenilin 1 (PS1) genotype 1/1 and late-onset Alzheimer's disease (AD).
With the increasing interest in apolipoprotein E (APOE) genetic testing to estimate the risk of developing late-onset Alzheimer disease, new educational tools are needed to help people make the best decision for themselves about whether to undergo this test.
With the exception of ApoE4, genome-wide association studies have failed to identify strong genetic risk factors for late-onset Alzheimer's disease, despite strong evidence of heritability, suggesting that many low penetrance genes may be involved.
While studies initially focused on its role in cholesterol and lipid metabolism, one apoE isoform (apoE4) is a major risk factor for development of late onset Alzheimer's disease.
While additional studies are needed, this study supports the association between the possibly protective GAB2 haplotype and the risk of late-onset AD in APOEε4 carriers.
While additional studies are needed, this study supports the association between the possibly protective GAB2 haplotype and the risk of late-onset AD in APOEε4 carriers.
When we analyzed haplotype distribution of the SNPs, taking into account the presence of the APOE allele, we observed a strong association between the ε4 allele and the GAC haplotype both in LOAD and FTLD patients.
When we analyzed haplotype distribution of the SNPs, taking into account the presence of the APOE allele, we observed a strong association between the ε4 allele and the GAC haplotype both in LOAD and FTLD patients.
When stratifying the sample by APOE one SNP (intergenic SNP rs11190302) was associated with LOAD in individuals lacking the epsilon4 allele (genotypic P = 0.027, allelic P = 0.066).
We validated the risk for LOAD with BIN1 (rs744373), CR1 (rs6656401), and ABCA7 (rs376465), as well as the protective association for MS4A6A (rs610932) and CLU (rs11136000) variants.
We validated the risk for LOAD with BIN1 (rs744373), CR1 (rs6656401), and ABCA7 (rs376465), as well as the protective association for MS4A6A (rs610932) and CLU (rs11136000) variants.
We validated the risk for LOAD with BIN1 (rs744373), CR1 (rs6656401), and ABCA7 (rs376465), as well as the protective association for MS4A6A (rs610932) and CLU (rs11136000) variants.
We validated the risk for LOAD with BIN1 (rs744373), CR1 (rs6656401), and ABCA7 (rs376465), as well as the protective association for MS4A6A (rs610932) and CLU (rs11136000) variants.
We therefore explore whether the six loci in Clusterin gene (CLU) (rs9331949), Lipoprotein lipase gene (LPL) (rs1059507, rs3200218, rs3208305, rs3735964) and Low-density lipoprotein receptor related protein 6 (LRP6) (rs2160525) could modulate LOAD risk through the alteration of miRNA binding sites.
We therefore explore whether the six loci in Clusterin gene (CLU) (rs9331949), Lipoprotein lipase gene (LPL) (rs1059507, rs3200218, rs3208305, rs3735964) and Low-density lipoprotein receptor related protein 6 (LRP6) (rs2160525) could modulate LOAD risk through the alteration of miRNA binding sites.
We suggest that this long transcript may alter the normal pathway for processing of amyloid precursor protein, the protein which appears to be central in the pathogenesis of AD.
We sought to examine the role of interactions between the nine recently identified AD susceptibility genes and APOE in cognitive function and decline in 1,153 participants from the Wisconsin Registry for Alzheimer's Prevention, a longitudinal study of middle-aged adults enriched for a parental history of AD.
We show that the APOE epsilon 4 allele frequency is increased only in the subset of patients who belong to families where LOAD secondary cases are present.
We show here that such an analysis can miss strong genetic association signals, such as that of the apolipoprotein-e gene in late-onset Alzheimer disease.