BACKGROUND: There are few studies on the long-term associations of physical activity (PA) to cognition. Here, we examine the association of midlife PA to late-life cognitive function and dementia. METHODS: The sample consisted of a population-based cohort of men and women (born in 1907-1935) participating in the Age Gene/Environment Susceptibility-Reykjavik Study. The interval between the midlife ascertainment of PA and late-life cognitive function was 26 years. Composite scores of speed of processing, memory, and executive function were assessed with a battery of neuropsychological tests, and dementia was diagnosed according to international guidelines. There were 4,761 nondemented participants and 184 (3.7%) with a diagnosis of dementia, with complete data for the analysis. RESULTS: Among the participants, no midlife PA was reported by 68.8%, 5 hours PA by 4.5%. Excluding participants with dementia compared with the no PA group, both PA groups had significantly faster speed of processing (5 hours, beta = .32, p trend < .0001), better memory (5 hours, beta = .18, p trend < .0001), and executive function (5 hours, beta = .18, p trend< .0001), after controlling for demographic and cardiovascular factors. The CONCLUSION: Midlife PA may contribute to maintenance of cognitive function and may reduce or delay the risk of late-life dementia.

BACKGROUND AND PURPOSE: Cerebral infarcts increase the risk for cognitive impairment. The relevance of location and number of infarcts with respect to cognitive function is less clear. METHODS: We studied the cross-sectional association between number and location of infarcts and cognitive performance in 4030 nondemented participants of the Age Gene/Environment Susceptibility-Reykjavik Study. Composite scores for memory, processing speed, and executive function were created from a neuropsychological battery. Subcortical, cortical, and cerebellar infarcts were identified on brain MRI. We performed linear regression analyses adjusted for demographic and vascular risk factors, depression, white matter lesions, and atrophy. RESULTS: Compared to participants with no infarcts, those with infarcts in multiple locations (n=287, 7%) had slower processing speed (beta=-0.19; PCONCLUSIONS: Having infarcts in >1 location is associated with poor performance in memory, processing speed, and executive function, independent of cardiovascular comorbidities, white matter lesions, and brain atrophy, suggesting that both the number and the distribution of infarcts jointly contribute to cognitive impairment.

Persons with type 2 diabetes are at increased risk of cognitive dysfunction. Less is known about which cognitive abilities are affected and how undiagnosed diabetes and impaired fasting glucose relate to cognitive performance. The authors explored this question using data from 1,917 nondemented men and women (average age = 76 years) in the population-based Age, Gene/Environment Susceptibility-Reykjavik Study (2002-2006). Glycemic status groups included diagnosed diabetes (self-reported diabetes or diabetic medication use; n = 163 (8.5%)), undiagnosed diabetes (fasting blood glucose >or=7.0 mmol/L without diagnosed diabetes; n = 55 (2.9%)), and impaired fasting glucose (fasting blood glucose 5.6-6.9 mmol/L; n = 744 (38.8%)). Composites of memory, processing speed (PS), and executive function were constructed from a neuropsychological battery. Linear regression was used to investigate cross-sectional differences in cognitive performance between glycemic groups, adjusted for demographic and health factors. Persons with diagnosed diabetes had slower PS than normoglycemics (beta = -0.12; P < 0.05); diabetes duration of >or=15 years was associated with significantly poorer PS and executive function. Undiagnosed diabetics had slower PS (beta = -0.22; P < 0.01) and poorer memory performance (beta = -0.22; P < 0.05). Persons with type 2 diabetes have poorer cognitive performance than normoglycemics, particularly in PS. Those with undiagnosed diabetes have the lowest cognitive performance.

BACKGROUND: Among persons with white matter lesions (WMLs), there is a range of cognitive function. We examine whether participation in leisure activities modifies the effect of WML load on cognitive function. METHODS: Data are from 2300 men and women (aged 66-92 years) participating in the population-based Age Gene/Environment Susceptibility-Reykjavik Study. Subcortical WML load was calculated as a weighted sum, based on size of lesions in the four lobes. Periventricular WML load was calculated as the sum of lesion scores, based on size, for the frontal caps, occipitoparietal caps and bands. The upper quartile of lesion load in either area was compared to the lower three quartiles. Composite scores of memory (MEM), speed of processing (SP), and executive function (EF) were constructed from a battery of neuropsychological tests. Frequency of participation in nine cognitively stimulating leisure activities was assessed via questionnaire; the upper quartile was compared to the lower three quartiles. Multiple regression, controlling for demographic and health factors and brain infarcts, was used to test the main effects and interaction of WMLs and leisure activity on cognitive function. RESULTS: High leisure activity was associated with higher performance in all three cognitive abilities: MEM beta = 0.20, 95% confidence interval [CI], 0.11-0.29; SP beta = 0.37, 95% CI, 0.29-0.45; and EF beta = 0.23, 95% CI, 0.15-0.29. High WML load was associated with significantly lower performance in SP (beta = -0.06, 95% CI, -0.13 to -0.01). The effect of WMLs on SP performance was modified by high leisure activity (p for interaction <.05). CONCLUSION: Participation in cognitively stimulating leisure activity may attenuate the effect of WML pathology on cognitive performance.