<b>Background:</b> Investigation on neurochemical changes in the frontal cortex in individuals with Alzheimer's disease (AD) and different Apolipoprotein E (APOE) genotypes, using <i>ex vivo</i> solid-state high-resolution NMR analysis, may lead to a better understanding of the neurochemistry associated with AD as well as new AD-specific metabolite biomarkers that might potentially improve the clinical diagnosis of AD.
<b>Background:</b> The apolipoprotein E epsilon4 (<i>ApoE</i> ε4) allele and female gender may be important risk factors for the development of Alzheimer's disease and amnestic mild cognitive impairment (aMCI).
<b>Conclusion:</b> These findings highlight a potential role of APOE ε4 status in affecting the association of hippocampus size with delayed recall memory in the early stage of AD.
<b>Methods:</b> Blood samples were provided from 110 individuals with ADFH to assess molecular biomarkers and the ApoE genotype for the purpose of dividing them into an ApoE-4 group (<i>n</i> = 16) and a non-ApoE-4 group (<i>n</i> = 16) in order for them to complete a visuospatial working memory task while simultaneously recording electroencephalographic signals.
<b>Theoretical background:</b> The Apolipoprotein E (APOE) ε4 genotype is known to be one of the strongest single-gene predictors for Alzheimer disease, which is characterized by widespread brain structural degeneration progressing along with cognitive impairment.
's analyses (Am J Epidemiol 2007;165:1231-1238) of how the apolipoprotein E *E4 allele, a well-documented risk factor for Alzheimer's disease, influences progression of cognitive impairments from mild or global cognitive impairment to dementia or death.
(1) To investigate atrophy patterns of hippocampal subfield volume and Alzheimer's disease (AD)-signature cortical thickness in mild cognitive impairment (MCI) patients; (2) to explore the association between the neuropsychological (NP) and the brain structure in the MCI and older normal cognition group; (3) to determine whether these associations were modified by the apolipoprotein E (APOE) ε4 gene and cognitive status.
(4) Despite a substantial effect of apolipoprotein E epsilon4 as a risk factor for AD, on decreasing the age at AD onset, and increasing the amount of cerebral amyloid angiopathy, its effect on senile plaque densities is variable and complex, being confounded with age, dementia severity, and methodologic differences.
(i) The risk of developing AD in our population was associated with the IL-1 beta (-511 C/T) promoter polymorphism; (ii) such risk was independent of the risk factor allele in the APOE gene (APOE4); and (iii) the IL-1 alpha promoter polymorphism (-889 C/T) was not associated with the disease.
1) APOEɛ4 genotype influences brain amyloid deposition pattern; 2) APOEɛ4 genotype does not modify Aβ biomarker cut-points estimated using unsupervised mixture modeling methods if white matter and brainstem references are used (but not when cerebellum is used as a reference); 3) findings of large differences in Aβ biomarker value differences based on APOE genotype are due to increased probability of having AD neuropathology and are most significant in mild cognitive impairment subjects; and 4) APOE genotype and age (but not gender) were associated with increased Aβ deposition rate.
1H magnetic resonance spectroscopy, cognitive function, and apolipoprotein E genotype in normal aging, mild cognitive impairment and Alzheimer's disease.
Alzheimer disease (AD) patients with both sporadic and familial forms of AD and non-demented controls were genotyped for common polymorphisms in the signal peptide for alpha-1-antichymotrypsin (ACT) gene and in two different regions of apolipoprotein E (APOE) gene.
Alzheimer's disease (AD) is a complex disease, involving multiple factors such as the production of aggregation-prone amyloid beta (Abeta) peptides, the formation of fibrillarly tangles of microtubule-associating proteins, Tau, and the polymorphism of cholesterol binding protein, APOE4.
Alzheimer's disease (AD) is highly prevalent in Wadi Ara despite the low frequency of apolipoprotein E ε4 in this genetically isolated Arab community in northern Israel.
Alzheimer's disease (AD) is most commonly detected during old age, but the underlying neuropathologic changes likely appear decades earlier, especially among patients possessing genetic risk factors, such as the isoform E4 of the apolipoprotein E (ApoE4).