Publications

Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia. The two pathological hallmarks of AD are the large extracellular plaques deposits of the β-amyloid peptides (Aβ) and the intraneuronal fibrillary tangles of the microtubule binding protein tau. The accumulation and aggregation of Aβ induce an inflammatory response followed by neuritic injury, hyperphosphorylation of tau protein and formation of fibrillary tangles, leading ultimately to neuronal dysfunction and cell death. Angiotensin-converting enzyme (ACE) is a dipeptidyl carboxypeptidase and a very important component of the renin–angiotensin system. ACE protein was found to be significantly increased in patients with AD and was shown to inhibit Aβ peptides aggregation in vitro. ACE has been extensively studied as a candidate gene for AD. ACE gene is located on chromosome 17q23, and has an insertion deletion polymorphism (I/D) of a 287 bp Alu repetitive sequence in intron 16. However, the association of ACE polymorphism with AD is still controversial. Some meta-analyses have shown that ACE I allele is a risk factor for AD. However, in other studies ACE D allele was associated with increased risk. Furthermore, few studies found no evidence to support linkage between ACE I/D polymorphism and AD. This study was performed to examine for the first time the association between ACE I/D polymorphism and the risk of AD in Lebanese patients. 45 patients diagnosed with AD and 48 age-matched controls were recruited. Patients and controls were tested for ACE I/D genotype by PCR. ACE genotype distribution in patients with AD was: 28.9% DD, 53.3% ID, and 17.8% II, while the controls showed 35.4% DD, 64.6% ID and 0% II. Hence, the II genotype was predominantly found in patients with AD. Therefore, our study suggests that the II genotype is associated with an increased risk of AD in the Lebanese population.