Cluster Analysis of Risk Factor Genetic Polymorphisms in Alzheimer’s Disease

• Published in: Neurochemical research Vol. 34; no. 1; pp. 23 - 28
• Main Authors: Randall, C. N., Strasburger, D., Prozonic, J., Morris, S. N., Winkie, A. D., Parker, G. R., Cheng, D., Fennell, E. M., Lanham, I., Vakil, N., Huang, J., Cathcart, H., Huang, R., Poduslo, S. E.
• Format: Journal Article
• Language: English
• Published: Boston Springer US 2009; Springer Nature B.V
• Subjects: Age of Onset; Aged; Aged, 80 and over; Alzheimer Disease - genetics; Amyloid Precursor Protein Secretases - genetics; Apolipoprotein E3 - genetics; Apolipoprotein E4 - genetics; Apolipoproteins E - genetics; Aspartic Acid Endopeptidases - genetics; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cathepsin D - genetics; Cell Biology; Cluster Analysis; Cystatin C - genetics; Female; Humans; Male; Middle Aged; Neurochemistry; Neurology; Neurosciences; Original Paper; Polymorphism, Genetic; Promoter Regions, Genetic - genetics; Receptors, LDL - genetics; Risk Factors; Sex Factors; Cluster analysis; Alzheimer’s disease; Genetic variants; Risk factors
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-008-9626-8

Multiple genetic variants may contribute to the risk of developing Alzheimer’s disease. We have analyzed polymorphisms in 9 genes to determine whether particular combinations would contribute to this risk. The genes were APOE, LDLr, CST3, CTSD, TNF, BACE1, MAPT, STH, eNOS, and TFCP2. Three risk groups for the disease were identified. Risk group I was younger, was heterozygous for the CST3 (GA), CTSD2936 (AG), TNF -308 (AG) genetic variants. Risk group II was older, was homozygous for the −427 APOE promoter polymorphism (TT), and heterozygous for the MAPT deletion and for the STH variant (QR). Group III had both the youngest and oldest subjects, were heterozygous for the −863 (AC) and −1031 (CT) TNF promoter polymorphisms. All three groups carried the APOE 4 allele and were heterozygous for both BACE1 polymorphisms. The control groups were carriers of the APOE 3 allele and were homozygous for the BACE1 genetic variants.