Simultaneous analysis of five genetic risk factors in Polish patients with Alzheimer's disease

• Published in: Neuroscience letters Vol. 344; no. 2; pp. 99 - 102
• Main Authors: Styczynska, Maria, Religa, Dorota, Pfeffer, Anna, Luczywek, Elzbieta, Wasiak, Boguslaw, Styczynski, Grzegorz, Peplonska, Beata, Gabryelewicz, Tomasz, Golebiowski, Marek, Kobrys, Malgorzata, Barcikowska, Maria
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 26.06.2003; Elsevier
• Subjects: Aged; alpha-Macroglobulins - genetics; Alzheimer Disease - genetics; Alzheimer's disease; Apolipoprotein E; Apolipoproteins E - genetics; Biological and medical sciences; Cathepsin D; Cathepsin D - genetics; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Gene Frequency; Genetic Testing; Humans; Male; Medical sciences; Medicin och hälsovetenskap; Myeloperoxidase; Neurology; Nitric oxide synthase; Nitric Oxide Synthase - genetics; Peroxidase - genetics; Poland; Polymorphism; Polymorphism, Genetic; Risk Factors; α2-Macroglobulin; Poland; Europe; α2-Macroglobulin; Apolipoprotein E; Myeloperoxidase; Nitric oxide synthase; Cathepsin D; Alzheimer's disease; Polymorphism; Human; Nervous system diseases; Alzheimer disease; Cerebral disorder; Central nervous system disease; Risk factor; Genetics; Degenerative disease
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(03)00438-5

As Alzheimer's disease (AD) is a complex disease, we decided to estimate how previously reported genetic polymorphisms interact to increase the risk for the disease. Five candidate genes were chosen: apolipoprotein E (APOE), α2-macroglobulin, cathepsin D, myeloperoxidase and nitric oxide synthase. Genotyping was performed in 100 cases of late-onset AD and 100 healthy controls. We found a highly significant difference in APOE ε4 distribution between groups ( P<0.005). However, no evidence of association for other studied loci was found. Cumulative analysis of five genetic polymorphisms was performed, but it also failed to reveal any synergistic effect of candidate genes greater than that caused by APOE itself. Our results suggest that the APOE ε4 allele is the only known genetic risk factor for late-onset, sporadic AD.