Further evidence of a lack of interaction between APOE and late-life blood pressure in predicting cognitive decline: The PATH Through Life Study (#211)
The apolipoprotien E(APOE) *e4 allele12 and hypertension34 are two of the most prevalent genetic and environmental risk factors associated with cognitive decline in latter life.Genetic and environmental risk factors, however, do not act in isolation and interactions between these risk factors may modify the rate of cognitive decline5 . The present analysis examines whether the APOE *e4 allelemoderates the association between late-life high blood pressure and cognition in later life. We tested whether and interaction between the blood pressure variables hypertension or mean arterial pressure and APOE genotype was associated with greater cognitive decline in early old age. Cognitive function was assed at three time points over a period of 8 years in 1,741 cognitively normal community-dwelling adults aged 60-64 years at baseline. Using multilevel models it was found that APOE genotype did moderate the association between late-life high blood pressure on some cognitive tests, however, the inclusion of the interaction term either did not significantly improve model fit or explain any additional variation in the models. These results suggest that APOE genotype does not moderate the association between late-life blood pressure and cognition in latter life.
- Small BJ, Rosnick CB, Fratiglioni L, Bäckman L (2004) Apolipoprotein E and Cognitive Performance: A Meta-Analysis. Psychology and Aging 19, 592–600
- Wisdom NM, Callahan JL, Hawkins KA (2011) The effects of apolipoprotein E on non-impaired cognitive functioning: A meta-analysis. Neurobiology of aging 32, 63–74
- Novak V, Hajjar I (2010) The relationship between blood pressure and cognitive function. Nat Rev Cardiol 7, 686–698
- Gasecki D, Kwarciany M, Nyka W, Narkiewicz K (2013) Hypertension, brain damage and cognitive decline. Curr Hypertens Rep 15, 547–558
- Payton A (2009) The Impact of Genetic Research on our Understanding of Normal Cognitive Ageing: 1995 to 2009. Neuropsychol Rev 19, 451–477