In this study, we investigate the impact of apolipoprotein E epsilon 4 (APOE ε4) as a major risk factor of Alzheimer's disease (AD), based on the clinical presentation of the disease in our population on the one hand, and comparison of the results with the findings from the literature on the other hand. Our study covered a population of 144 patients versus 90 healthy controls matched with each other in terms of age, gender, age of onset, etc. All patients underwent neurological examination, comprehensive neuropsychological assessment and brain magnetic resonance imaging.
View Article and Find Full Text PDFIt is widely recognized that Alzheimer's disease (AD) is the main cause of dementia in the elderly. AD is typically characterized by the extraneuronal plaque made up essentially of the amyloid β peptide and intraneuronal tangles of hyperphosphorylated microtubule-associated protein. This study investigates the possible interaction between AD and the deletion/insertion polymorphism in intron 9 of the gene haplotype and state in a Tunisian AD cases population (n = 85) and control (n = 91).
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with an as yet poorly understood etiology. Both environmental and genetic factors have been implicated as predisposing factors. The apolipoprotein E (APOE) ɛ4 allele is an established genetic susceptibility factor for AD for several populations including the Tunisian population.
View Article and Find Full Text PDFAngiotensin-converting enzyme (ACE) has shown altered activity in patients with neurological diseases. An insertion/deletion (I/D) polymorphism of the ACE gene encoding angiotensin-converting enzyme has been reported to be associated with the risk for Alzheimer's disease (AD), and is generally considered to be a disorder primarily affecting memory. We conducted a case-control study in a sample composed of 85 sporadic AD patients and 90 age- and sex-matched controls to investigate the possible effect of the polymorphism and cognitive profile.
View Article and Find Full Text PDFA minority of Alzheimer disease (AD) patients begin presenting symptoms before the age of 65 years. A familial aggregation is often found in this group of early-onset AD, and, in a subset of families, the pattern of inheritance is consistent with autosomal dominant inheritance. Fully penetrant variants in amyloid precursor protein, presenilin 1 (PSEN1), and presenilin 2 are the only causative mutations reported for autosomal dominant AD.
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