TY - JOUR
T1 - Neuroprotective lifestyles and the aging brain
T2 - Activity, atrophy, and white matter integrity
AU - Gow, Alan J.
AU - Bastin, Mark E.
AU - Maniega, Susana Munoz
AU - Hernandez, Maria C. Valdes
AU - Morris, Zoe
AU - Murray, Catherine
AU - Royle, Natalie A.
AU - Starr, John M.
AU - Deary, Ian J.
AU - Wardlaw, Joanna M.
PY - 2012/10
Y1 - 2012/10
N2 - Objectives: Increased participation in leisure and physical activities may be cognitively protective. Whether activity might protect the integrity of the brain's white matter, or reduce atrophy and white matter lesion (WML) load, was examined in the Lothian Birth Cohort 1936 (n = 691), a longitudinal study of aging.
Methods: Associations are presented between self-reported leisure and physical activity at age 70 years and structural brain biomarkers at 73 years. For white matter integrity, principal components analysis of 12 major tracts produced general factors for fractional anisotropy (FA) and mean diffusivity. Atrophy, gray and normal-appearing white matter (NAWM) volumes, and WML load were assessed using computational image processing methods; atrophy and WML were also assessed visually.
Results: A higher level of physical activity was associated with higher FA, larger gray and NAWM volumes, less atrophy, and lower WML load. The physical activity associations with atrophy, gray matter, and WML remained significant after adjustment for covariates, including age, social class, and health status. For example, physical activity (standardized beta = -0.09, nonstandardized beta = -0.09, p = 0.029) and stroke (standardized beta = 0.18, nonstandardized beta = 0.69, p = 0.003) each had an independent effect on rated WML load. Leisure activity was associated with NAWM volume, but was nonsignificant after including covariates.
Conclusions: In this large, narrow-age sample of adults in their 70s, physical activity was associated with less atrophy and WML. Its role as a potential neuroprotective factor is supported; however, the direction of causation is unclear from this observational study. Neurology (R) 2012;79:1802-1808
AB - Objectives: Increased participation in leisure and physical activities may be cognitively protective. Whether activity might protect the integrity of the brain's white matter, or reduce atrophy and white matter lesion (WML) load, was examined in the Lothian Birth Cohort 1936 (n = 691), a longitudinal study of aging.
Methods: Associations are presented between self-reported leisure and physical activity at age 70 years and structural brain biomarkers at 73 years. For white matter integrity, principal components analysis of 12 major tracts produced general factors for fractional anisotropy (FA) and mean diffusivity. Atrophy, gray and normal-appearing white matter (NAWM) volumes, and WML load were assessed using computational image processing methods; atrophy and WML were also assessed visually.
Results: A higher level of physical activity was associated with higher FA, larger gray and NAWM volumes, less atrophy, and lower WML load. The physical activity associations with atrophy, gray matter, and WML remained significant after adjustment for covariates, including age, social class, and health status. For example, physical activity (standardized beta = -0.09, nonstandardized beta = -0.09, p = 0.029) and stroke (standardized beta = 0.18, nonstandardized beta = 0.69, p = 0.003) each had an independent effect on rated WML load. Leisure activity was associated with NAWM volume, but was nonsignificant after including covariates.
Conclusions: In this large, narrow-age sample of adults in their 70s, physical activity was associated with less atrophy and WML. Its role as a potential neuroprotective factor is supported; however, the direction of causation is unclear from this observational study. Neurology (R) 2012;79:1802-1808
KW - FITNESS
KW - TRACTOGRAPHY
KW - OLD-AGE
KW - MRI
KW - EXERCISE
KW - BIRTH COHORT 1936
KW - PHYSICAL-ACTIVITY
KW - SEGMENTATION
KW - IMAGES
KW - COGNITION
U2 - 10.1212/WNL.0b013e3182703fd2
DO - 10.1212/WNL.0b013e3182703fd2
M3 - Article
C2 - 23091073
SN - 0028-3878
VL - 79
SP - 1802
EP - 1808
JO - Neurology
JF - Neurology
IS - 17
ER -