Association between APOE Genotype and Change in Physical Function in a Population-Based Swedish Cohort of Older Individuals Followed Over Four Years
Artikel i vetenskaplig tidskrift, 2016
The association between decline in physical function and age-related conditions, such as reduced cognitive performance and vascular disease, may be explained by genetic influence on shared biological pathways of importance for aging. The apolipoprotein F (APOE) gene is well-known for its association with Alzheimer's disease, but has also been related to other disorders of importance for aging. The aim of this study was to investigate possible associations between APOE allele status and physical function in a population-based longitudinal study of older individuals. In 2005, at the age of 75, 622 individuals underwent neuropsychiatric and physical examinations, including tests of physical function, and APOE-genotyping. Follow-up examinations were performed at age 79. A significantly larger decline in grip strength (p = 0.015) between age 75 and 79 was found when comparing APOE epsilon 4 allele carriers with non carriers [10.3 (+/- 10.8) kg versus 7.8 (+/- 10.1) kg]. No association was seen with decline in gait speed, chair-stand, or balance. The association with grip strength remained after correction for cognitive and educational level, depression, cardiovascular disease, stroke, and BMI.
alzheimers-disease
grip strength
cognitive decline
dementia
Geriatrics & Gerontology
gait speed
APOE epsilon 4 allele
women
adults
allele
Neurosciences & Neurology
prevalence
apolipoprotein-e polymorphism
risk
grip strength
performance
physical function
Författare
Ingmar Skoog
Göteborgs universitet
Helena M Hörder
Göteborgs universitet
Kerstin Frändin
Göteborgs universitet
Lena Johansson
Göteborgs universitet
Svante Östling
Göteborgs universitet
Kaj Blennow
Göteborgs universitet
Henrik Zetterberg
Göteborgs universitet
Anna Håkansson
Göteborgs universitet
Frontiers in Aging Neuroscience
1663-4365 (ISSN)
Vol. 8 Article number: 225-Ämneskategorier
Klinisk medicin
DOI
10.3389/fnagi.2016.00225