TNK1
Non-receptor tyrosine-protein kinase TNK1 (EC 2.7.10.2) (CD38 negative kinase 1)
PublicationsПравить
Healthy and impaired cognitive aging may be associated to different prevalences of single-nucleotide polymorphisms (SNPs). In a multicenter case-control association study, we studied the SNPs rs11136000 (clusterin, CLU), rs541458 (phosphatidylinositol binding clatrin assembly protein, PICALM), and rs1554948 (transcription factor A, and tyrosine kinase, non-receptor, 1, TNK1) according to the three age groups 50-65 years (group 1), 66-80 years (group 2), and 80 years (group 3) in 569 older subjects without cognitive impairment (NoCI) and 520 Alzheimer's disease (AD) patients. In NoCI subjects, a regression analysis suggested a relationship between age and TNK1 genotypes, with the TNK1-A/A genotype frequency that increased with higher age, and resulting in a different distribution of the TNK1-A allele. In AD patients, a regression analysis suggested a relationship between age and PICALM genotypes and TNK1 genotypes, with the PICALM-T/C and TNK1-A/A genotype frequencies that decreased with increasing age. A resulting difference in the distribution of PICALM-C allele and TNK1-A allele was also observed. The TNK1-A allele was overrepresented in NoCI subjects than in AD patients in age groups 2 and 3. These results confirmed after adjustment for apolipoprotein E polymorphism, which suggested a different role of PICALM and TNK1 in healthy and impaired cognitive aging. More studies, however, are needed to confirm the observed associations.
MeSH Terms
- Aged
- Aged, 80 and over
- Aging
- Alleles
- Alzheimer Disease
- Clusterin
- Cohort Studies
- Female
- Fetal Proteins
- Gene Frequency
- Genetic Predisposition to Disease
- Humans
- Male
- Middle Aged
- Monomeric Clathrin Assembly Proteins
- Polymorphism, Single Nucleotide
- Protein-Tyrosine Kinases
Keywords
- Alzheimer’s disease
- Biogerontology
- Brain aging
- Cognition
- Dementia
- Genetics