OBJECTIVETo examine the effects of baseline and incident diabetes on change in cognitive function over 12 years.RESEARCH DESIGN AND METHODSA sample of 1,290 individuals aged ≥40 years at baseline, participating in the Maastricht Aging Study, were cognitively tested at baseline, after 6 years, and after 12 years. Of these, 68 participants had type 2 diabetes at baseline, and 54 and 57 had incident diabetes at the 6- and 12-year follow-up, respectively. Changes in performance on tests of information-processing speed, executive function, and verbal memory from baseline to 6- and 12-year follow-up were compared between groups using linear mixed models. Effects of diabetes on cognitive decline were adjusted for demographic variables, history of smoking, alcohol intake, and comorbid conditions, including hypertension, cardiovascular disease, BMI, and depression.RESULTSParticipants with baseline diabetes showed larger decline in information-processing speed (estimate −7.64; P < 0.01), executive function (21.82; P < 0.01), and delayed word recall (−1.35; P < 0.05) over the 12-year follow-up compared with control subjects. No significant difference in decline was observed for immediate word recall. Compared with control subjects, participants with incident diabetes showed subtle early decline in information-processing speed only. Interestingly, they did not show larger decline in any other cognitive domain.CONCLUSIONSIndividuals with baseline type 2 diabetes show accelerated cognitive decline, particularly in information-processing speed and executive function, compared with individuals without diabetes. In incident diabetes, decline in speed becomes detectable first, and cognitive decline seems to increase with increasing exposure time.

245I dentifying modifiable risk factors for cognitive decline and dementia is crucial to effective preventive strategies. Known risk factors include age, education, physical activity, diet, depression, and vascular disease.1 Although the dementia prevalence increases exponentially from 65 years of age, the risk builds up gradually with critical periods for some exposures across the life span. 2Cognitive decline from previous levels of functioning is a core criterion for the diagnosis of dementia.3 Findings from observational studies suggest that hypertension is a major risk factor for accelerated cognitive decline 4 and dementia. 5Hypertension predicts decline in the domains of memory, attention, 6 psychomotor speed, 7 and other fluid abilities. 8The effect of hypertension seems to be age dependent for the associations with cognitive decline and dementia 9 : Studies into midlife hypertension have generally found positive associations, 8,10,11 whereas studies into late life hypertension are more likely to show mixed results of a risk increasing, no, or even a protective effect. 8,12 Prospective studies with exceptionally long follow-up duration suggest an inverted U-shaped trajectory of blood pressure (BP) over time in people who later develop dementia (ie, an increase from midlife to late life and declining levels thereafter). 13,14 Understanding the effect of hypertension on cognitive decline and dementia is important because it opens the possibility of risk management using available interventions. 15,16 Observational studies have shown that individuals with pharmacologically controlled hypertension decline less than people with uncontrolled or untreated hypertension.4 Meta-analysis of randomized clinical trials found a significant dementia risk reduction in trials that prescribed diuretics or calcium channel blockers in the treatment arm, although no generic effect of hypertension medication was found. 17Most might be gained from timely interventions in newly diagnosed hypertension cases, but, to the best of our knowledge, no study has focused on the onset and course of cognitive decline in incident hypertension. One previous study of 49 healthy older adults used incident hypertension as a covariate when studying risk for white matter lesion progression on cognitive impairment (average follow-up, 5.6 years).18 ItAbstract-Midlife hypertension is a risk factor for dementia, but little is known about the cognitive trajectories of individuals with incident hypertension. This study follows the cognitive functioning in prevalent and incident hypertension for 12 years and in relation to age and treatment status. Cognitively intact adults aged 25 to 84 years (n=1805) were serially assessed at baseline, 6 years, and 12 years. Hypertension was defined by sphygmomanometry or antihypertensive medication use, and its association with cognitive decline was tested in random-effects models. At baseline, 638 (35.3%) participants had hypertension. They showed faster decline in memory (χ 2 test for homogeneity=35.75; df=2; P<0....

Background/Objective: studies on the association of dementia with specific body composition (BC) components are scarce. Our aim was to investigate associations of BC measures with different levels of cognitive function in late-life. Methods: we studied 5,169 participants (mean age 76 years, 42.9% men) in the AGES-Reykjavik Study of whom 485 (9.4%) were diagnosed with mild cognitive impairment (MCI) and 307 (5.9%) with dementia. Visceral fat, abdominal and thigh subcutaneous fat, and thigh muscle were assessed by computed tomography. MCI and dementia were based on clinical assessment and a consensus meeting; those without MCI or dementia were categorised as normal. Multinomial regression models assessed the associations stratified by sex and in additional analyses by midlife body mass index (BMI). Results: among women, there was a decreased likelihood of dementia per SD increase in abdominal subcutaneous fat (OR 0.72; 95% CI: 0.59-0.88), thigh subcutaneous fat (0.81; 0.67-0.98) and thigh muscle (0.63; 0.52-0.76), but not visceral fat, adjusting for demographics, vascular risk factors, stroke and depression. Inverse associations of fat with dementia were attenuated by weight change from midlife and were strongest in women with midlife BMI <25. In men, one SD increase in thigh muscle was associated with a decreased likelihood of dementia (0.75; 0.61-0.92). BC was not associated with MCI in men or women. Conclusion: a higher amount of abdominal and thigh subcutaneous fat were associated with a lower likelihood of dementia in women only, while more thigh muscle was associated with a lower likelihood of dementia in men and women.

We found inverse associations of SAF (a noninvasive marker for tissue AGEs) with cognitive performance, which were attenuated after adjustment for vascular risk factors and depression.