Polymorphism of glycogen synthase kinase 3 Beta and cyclindependent kinase 5 genes in early and late onset Alzheimers disease

• Autorzy: Niwinska J.M. , Markiewicz P. , Styczynska M. , Czapski G.A. , Barcikowska M. , Strosznajder J.B.
• Języki publikacji: EN

Abstrakty

EN

Alzheimerís disease (AD) is the main cause of dementia in the elderly. Over-activation of Glycogen Synthase Kinase 3 beta and Cyclin-Dependent Kinase 5 has been implicated in the aberrant phosphorylation of tau ñ the major component of the neurofi brillary tangles, which besides deposits of amyloid β are pathological hallmarks of AD. In this study we assessed the association between single nucleotide polymorphism (SNP) in those kinases genes and the risk of early (EOAD) and late onset (LOAD) Alzheimerís disease. TaqMan SNP genotyping assay or polymerase chain reactionrestriction fragments length polymorphism (PCR-RFLP) assay were used to genotype 4 SNP sites in 198 Polish LOAD cases, 71 EOAD cases and 104 controls. The distribution of genotypes in rs334558 SNP in GSK3β gene signifi cantly differed between patients with late onset AD and aged related, healthy control group. No signifi cant association between rs9278, rs2069454 and rs2069442 SNPs in CDK5 gene and AD was found and none of the examined alleles can be considered now as a genetic risk factor in AD in Polish population. The analysis of environmental factors showed higher serum level of total cholesterol and lower LDL (low density lipoprotein) level in EOAD and LOAD groups compared to control group. Moreover lower level of vitamin B12 and higher homocysteine level were observed only in LOAD group compared to controls. This study was supported MS&HE scientifi c network 28/E-32/SN0053/2007

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2009
• Tom: 69
• Numer: 1
• Opis fizyczny: p.91

Twórcy

autor

Niwinska J.M.

• Department of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Markiewicz P.

• Department of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Styczynska M.

• Department of Neurodegenerative Disorders, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Czapski G.A.

• Department of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Barcikowska M.

• Department of Neurodegenerative Disorders, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

autor

Strosznajder J.B.

• Department of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland