It 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.
View Article and Find Full Text PDFThe apolipoprotein E (APOE) is a well-established risk factor for late-onset Alzheimer's disease (AD). Several studies have attempted to confirm the association between the polymorphism located at position -491 in the transcriptional regulatory region of the APOE gene and AD. We examined in 85 AD patients and 90 control subjects of a Tunisian population the potential involvement of this polymorphism as a risk factor for AD, either through an independent effect or through interaction with the existing APOE ε4 allele risk.
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