Najiba Fekih-Mrissa1, Sarra Klai2, Meriem Mrad2, Malek Mansour3, Jamel Zaouali3, Nasreddine Gritli4, Ridha Mrissa3. 1. Laboratoire de Biologie Moléculaire, Service d'Hématologie, Hôpital Militaire Principal d'Instruction de Tunis, Montfleury, Tunis, Tunisie; Académie Militaire Fondouk Jédid, Nabeul, Tunisie. Electronic address: fnajiba@yahoo.fr. 2. Laboratoire de Biologie Moléculaire, Service d'Hématologie, Hôpital Militaire Principal d'Instruction de Tunis, Montfleury, Tunis, Tunisie; Faculté des Sciences de Tunis, Université de Tunis El Manar, El Manar, Tunisie. 3. Service de Neurologie, Hôpital Militaire Principal d'Instruction de Tunis, Montfleury, Tunis, Tunisie; Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis, Tunisie. 4. Laboratoire de Biologie Moléculaire, Service d'Hématologie, Hôpital Militaire Principal d'Instruction de Tunis, Montfleury, Tunis, Tunisie; Faculté de Pharmacie, Université de Monastir, Monastir, Tunisie.
Abstract
BACKGROUND: The ɛ4 allele of the apolipoprotein E (APOE) gene is a well-characterized genetic risk factor for Alzheimer disease (AD). The association between stroke and a higher risk for AD has also been reported. Our study sought to determine the relationship between the APOE gene and AD and the comorbid risk of stroke. METHODS: The subjects of this study consisted of 48 patients with AD and 48 members of a control group. All subjects were genotyped for APOE. RESULTS: The results clearly show a significant increased risk of AD in carriers of the APOE ε3/ε4 genotype (P = .003, odds ratio [OR] = 4.1) or ε4 allele (P = .001, OR = 4.2). The risk for stroke in AD patients was also increased for carriers of the APOE ε3/ε4 genotype (P = .02, OR = 9.0) and for carriers of the APOE ε4 allele (P = .004, OR = 5.5). CONCLUSIONS: The present study is the first to establish a relationship between APOE ε4 and concomitant AD and stroke in the Tunisian population.
BACKGROUND: The ɛ4 allele of the apolipoprotein E (APOE) gene is a well-characterized genetic risk factor for Alzheimer disease (AD). The association between stroke and a higher risk for AD has also been reported. Our study sought to determine the relationship between the APOE gene and AD and the comorbid risk of stroke. METHODS: The subjects of this study consisted of 48 patients with AD and 48 members of a control group. All subjects were genotyped for APOE. RESULTS: The results clearly show a significant increased risk of AD in carriers of the APOE ε3/ε4 genotype (P = .003, odds ratio [OR] = 4.1) or ε4 allele (P = .001, OR = 4.2). The risk for stroke in ADpatients was also increased for carriers of the APOE ε3/ε4 genotype (P = .02, OR = 9.0) and for carriers of the APOE ε4 allele (P = .004, OR = 5.5). CONCLUSIONS: The present study is the first to establish a relationship between APOE ε4 and concomitant AD and stroke in the Tunisian population.