APOE ε4 is associated with longer telomeres, and longer telomeres among ε4 carriers predicts worse episodic memory
2012 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 33, no 2, 335-344 p.Article in journal (Refereed) Published
Both leukocyte telomere length and the apolipoprotein ε4 allele have been associated with mortality, cardiovascular disease, cognition, and dementia. The authors investigated whether leukocyte telomere length was associated with APOE genotype or cognitive abilities in the context of APOE genotype. The setting for this cross-sectional study was 427 nondemented individuals aged 41–81 yr. The authors found that ε4 carriers overall exhibited significantly longer telomeres compared with non-carriers (difference of 268 bp, p = 0.001). This difference was greatest at the lower limit of the age span and nonsignificant at the upper limit, which translated into a significantly higher telomere attrition rate (p = 0.049) among ε4 carriers (37 bp/years) compared with non-carriers (21 bp/year). Further, longer telomeres among ε4 carriers significantly predicted worse performance on episodic memory tasks. No significant associations were found on tasks tapping semantic and visuospatial ability, or among ε3/ε3 carriers. In conclusion, APOE ε4 carriers had longer telomeres compared with non-carriers, but higher rate of attrition. Among them, longer telomeres predicted worse performance on episodic memory tasks. These observations suggest that the ε4 allele is associated with abnormal cell turnover of functional and possibly clinical significance.
Place, publisher, year, edition, pages
Elsevier, 2012. Vol. 33, no 2, 335-344 p.
APOE, cognition, telomere length
Research subject Psychology
IdentifiersURN: urn:nbn:se:su:diva-74227DOI: 10.1016/j.neurobiolaging.2010.03.004ISI: 000298171800012OAI: oai:DiVA.org:su-74227DiVA: diva2:507261
The research was funded by the Swedish Research Council (grant 2,006–4,472), the Medical Faculty, Umeå University, and the County Councils of Västerbotten and Norrbotten, Sweden. The Betula Study is supported by Grants 345-2003-3883 and 315-2004-6977 from the Swedish Research Council. The APOE genotyping was funded by the Fund for Scientific Research – Flanders (FWO-V). K S. Is holder of a postdoctoral fellowship of the FWO-V. Research nurses Annelie Nordin and Eva Lundberg are thankfully acknowledged for their help and expertise. We also acknowledge the statistical expertise of Birgitta Törnkvist (Department of Statistics, Umeå University).2012-03-022012-03-022012-05-31Bibliographically approved