The aim of the present work is to investigate the usefulness of cerebrospinal fluid (CSF) beta-amyloid protein (Abeta1-42) and total tau protein (t-tau) analyses in the diagnosis of AD and whether apolipoprotein E (ApoE) epsilon4 allele is a factor for AD affecting Tunisian people.
A luteinizing hormone receptor intronic variant is significantly associated with decreased risk of Alzheimer's disease in males carrying an apolipoprotein E epsilon4 allele.
We have studied the impact of the apolipoprotein E gene (APOE) on the chromosome 19 linkage peak from an analysis of sib-pairs affected by Alzheimer's disease.
Because the structural and biophysical properties of a protein determine how it functions under normal and abnormal conditions, apoE4, with its multiple cellular origins and multiple structural and biophysical properties, might contribute to the pathology of AD through several different mechanisms.
The apoE4 allele is a major risk factor for late-onset familial and sporadic Alzheimer's disease (AD) and is associated with a poor outcome after brain injury.
Although the mechanisms underlying apoE4's action in AD pathogenesis are still poorly understood, emerging data strongly suggest that apoE4 contributes to this disease by interacting with different factors through various pathways.
We have described the allele frequencies of the apolipoprotein E gene (APOE) in a large population of patients with AD compared to the frequencies in a cognitively-normal control group, and estimated the effect of the APOE epsilon4 allele on the risk and the age at onset of AD in this population.
There was a significant interaction between cholesterol, APOE-epsilon4, and the risk of Alzheimer disease (AD) in the Yoruba, a population that has lower cholesterol levels and lower incidence rates of AD compared to African Americans.
We have previously reported the isoform-specific interaction of native human apolipoprotein E (APOE, gene; apoE, protein) epsilon 3 with the amyloid-ss peptide, Ass(1-40), the major component of the cerebral amyloid deposits that appear to cause Alzheimer's disease.