Physical activity may help maintain cognitive function and decrease dementia risk, but epidemiological findings remain controversial. The aim of our study was to investigate the association between ...leisure-time physical activity at midlife and the subsequent development of dementia and Alzheimer's disease (AD).
Participants were randomly selected from the survivors of a population-based cohort previously surveyed in 1972, 1977, 1982, or 1987. 1449 persons (72·5%) age 65–79 years participated in the re-examination in 1998 (mean follow-up, 21 years). 117 persons had dementia and 76 had AD. Multiple logistic regression methods were used to analyse the association between leisure-time physical activity and dementia or AD.
Leisure-time physical activity at midlife at least twice a week was associated with a reduced risk of dementia and AD (odds ratio OR 0·48 95% CI 0·25–0·91 and 0·38 0·17–0·85, respectively), even after adjustments for age, sex, education, follow-up time, locomotor disorders,
APOE genotype, vascular disorders, smoking, and alcohol drinking. The associations were more pronounced among the
APOE ɛ4 carriers.
Leisure-time physical activity at midlife is associated with a decreased risk of dementia and AD later in life. Regular physical activity may reduce the risk or delay the onset of dementia and AD, especially among genetically susceptible individuals.
Magnetic resonance imaging (MRI) has been suggested as a useful tool in early diagnosis of Alzheimer’s disease (AD). Based on MRI-derived volumes, we studied the hippocampus and entorhinal cortex ...(ERC) in 59 controls, 65 individuals with mild cognitive impairment (MCI) and 48 patients with AD. The controls and individuals with MCI were derived from population-based cohorts. Volumes of the hippocampus and ERC were significantly reduced in the following order: control>MCI>AD. Stepwise discriminant function analysis showed that the most efficient overall classification between controls and individuals with MCI subjects was achieved with ERC measurements (65.9%). However, the best overall classification between controls and AD patients (90.7%), and between individuals with MCI and AD patients (82.3%) was achieved with hippocampal volumes. Our results suggest that the ERC atrophy precedes hippocampal atrophy in AD. The ERC volume loss is dominant over the hippocampal volume loss in MCI, whereas more pronounced hippocampal volume loss appears in mild AD.
Recent research has shown an increased rate of conversion to dementia in subjects with mild cognitive impairment (MCI) compared to controls. However, there are no specific methods to predict who will ...later develop dementia. In the present study, 22 controls and 56 MCI subjects were followed on average for 37 months (max. 60 months) and studied with magnetic resonance imaging (MRI) at baseline to assess changes in brain structure associated to later progression to dementia. Voxel-based morphometry (VBM) was used to investigate gray matter atrophy. During the follow-up, 13 subjects progressed to dementia. At baseline, no differences were detected in age or education between the control and MCI subjects, but they differed by several neuropsychological tests. The stable and progressive MCI subjects differed only by CDR sum of boxes scores and delayed verbal recall, which were also significant predictors of conversion to dementia. At the baseline imaging, the MCI subjects showed reduced gray matter density in medial temporal, temporoparietal as well as in frontal cortical areas compared to controls. Interestingly, the progressive MCI subjects showed atrophy in the left temporoparietal and posterior cingulate cortices and in the precuneus bilaterally, and a trend for hippocampal atrophy when compared to the stable MCI subjects. We conclude that widespread cortical atrophy is present already two and a half years before a clinical diagnosis of dementia can be set.
Abstract Objective: To examine the relation of midlife raised blood pressure and serum cholesterol concentrations to Alzheimer's disease in later life. Design: Prospective, population based study. ...Setting: Populations of Kuopio and Joensuu, eastern Finland. Participants: Participants were derived from random, population based samples previously studied in a survey carried out in 1972, 1977, 1982, or 1987. After an average of 21 years' follow up, a total of 1449 (73%) participants aged 65–79 took part in the re-examination in 1998. Main outcome measures: Midlife blood pressure and cholesterol concentrations and development of Alzheimer's disease in later life. Results: People with raised systolic blood pressure (≥160 mm Hg) or high serum cholesterol concentration (≥6.5 mmol/l) in midlife had a significantly higher risk of Alzheimer's disease in later life, even after adjustment for age, body mass index, education, vascular events, smoking status, and alcohol consumption, than those with normal systolic blood pressure (odds ratio 2.3, 95% confidence interval 1.0 to 5.5) or serum cholesterol (odds ratio 2.1, 1.0 to 4.4). Participants with both of these risk factors in midlife had a significantly higher risk of developing Alzheimer's disease than those with either of the risk factors alone (odds ratio 3.5, 1.6 to 7.9). Diastolic blood pressure in midlife had no significant effect on the risk of Alzheimer's disease. Conclusion: Raised systolic blood pressure and high serum cholesterol concentration, and in particular the combination of these risks, in midlife increase the risk of Alzheimer's disease in later life. What is already known on this topic Vascular risk factors may play an important part as risk factors for Alzheimer's disease No population based studies have evaluated prospectively the impact of both midlife blood pressure and cholesterol concentration in both men and women on the subsequent development of Alzheimer's disease What this study adds Raised systolic blood pressure and high serum cholesterol concentration, and in particular the combination of these risks, in midlife increased the risk of Alzheimer's disease in later life Raised systolic blood pressure and hypercholesterolaemia may have a role in the pathogenesis of Alzheimer's disease; more emphasis should be placed on identification and appropriate treatment of these conditions
Abstract The concept of mild cognitive impairment (MCI) has been proposed to represent a transitional stage between normal aging and dementia. We studied the predictive value of the MRI-derived ...volumes of medial temporal lobe (MTL) structures, white matter lesions (WML), neuropsychological tests, and Apolipoprotein E (APOE) genotype on conversion of MCI to dementia and AD. The study included 60 subjects with MCI identified from population cohorts. During the mean follow-up period of 34 months, 13 patients had progressed to dementia (9 to Alzheimer's disease (AD)). In Cox regression analysis the baseline volumes of the right hippocampus, the right entorhinal cortex and CDR sum of boxes predicted the progression of MCI to dementia during the follow-up. In a bivariate analysis, only the baseline volumes of entorhinal cortex predicted conversion of MCI to AD. The Mini-Mental State Examination (MMSE) score at baseline, WML load, or APOE genotype were not significant predictors of progression. The MTL volumetry helps in identifying among the MCI subjects a group, which is at high risk for developing AD.
To test the hypothesis that metabolic syndrome predicts cognitive impairment, and to examine the association of single metabolic risk factors with cognitive functioning.
We performed a 12-year ...follow-up study in a population-based sample of 101 women aged 60-70 years at baseline. Metabolic syndrome was defined by the National Cholesterol Education Program criteria (> or =3 out of 5 risk factors). Global cognitive function was measured by the Mini-Mental State Examination both at baseline and follow-up. A detailed neuropsychological evaluation for memory and cognitive speed was performed at follow-up.
The prevalence of metabolic syndrome increased from 13% at baseline to 49% at follow-up (p < 0.001). Women with metabolic syndrome at baseline had a 4.27 (95% confidence interval: 1.02-17.90; p = 0.047) times higher risk of poor memory at follow-up after adjustment for age, education and depression. The increasing number of metabolic risk factors was associated with worsening of memory at follow-up (p = 0.034 for linear trend). Women with low baseline levels of high-density lipoprotein (HDL) cholesterol were more likely to have poor memory at follow-up than those with higher HDL levels (p = 0.028). The risk of having poor memory increased by 46.5% (95% confidence interval: 15-66%; p = 0.008) with 1 SD decrease in HDL cholesterol level.
In elderly women, metabolic syndrome may be an important contributor to worsening of memory, which is an essential part of mild cognitive impairment.
Abstract Objective To evaluate the relation between midlife alcohol consumption and mild cognitive impairment and dementia in old age, and the possible modification of this relation by apolipoprotein ...E. Design Prospective, population based study. Setting Populations of Kuopio and Joensuu, eastern Finland. Participants Of 1464 men and women aged 65-79 years randomly selected from population based samples studied in 1972 or 1977, 1018 (70%) were re-examined in 1998 (after an average follow up of 23 years). Main outcome measures Mild cognitive impairment and dementia in old age. Results Participants who drank no alcohol at midlife and those who drank alcohol frequently were both twice as likely to have mild cognitive impairment in old age as those participants who drank alcohol infrequently. The risk of dementia related to alcohol drinking was modified by the presence of the apolipoprotein e4 allele. The carriers of apolipoprotein e4 had an increased risk of dementia with increasing alcohol consumption: compared with non-carriers who never drank, the odds ratio for carriers who never drank was 0.6, for infrequent drinkers it was 2.3, and for frequent drinkers was 3.6 (the overall interaction term “drinking frequency*apolipoprotein e4” was significant (P = 0.04), as were the interactions “infrequent drinking*apolipoprotein e4” (P = 0.02) and “frequent drinking*apolipoprotein e4” (P = 0.03)). Non-carriers of apolipoprotein e4 had similar odds ratios for dementia irrespective of alcohol consumption. Conclusion Alcohol drinking in middle age showed a U shaped relation with risk of mild cognitive impairment in old age. Risk of dementia increased with increasing alcohol consumption only in those individuals carrying the apolipoprotein e4 allele.
Background Risk of dementia and Alzheimer's disease is higher among adults with limited education, and the less educated perform poorer on cognitive function tests. This study determines whether the ...socioeconomic environment experienced during childhood has an impact on cognitive functioning in middle age. Methods A population-based study of eastern Finnish men (n = 496) aged 58 and 64 for whom there were data on parent's socioeconomic position (SEP), their own education level, and performance on neuropsychological tests. Cognitive function was measured using the Trail Making Test, the Selective Reminding Test, the Verbal Fluency Test, the Visual Reproduction Test, and the Mini Mental State Exam. Results We found a significant and graded association between parental SEP (combined as an index) and cognitive function both prior to and after adjustment for respondent's education. Those from more disadvantaged backgrounds exhibited the poorest performance. When the separate components of the parental SEP measure were used, father's occupation and mother's education were independently associated with the respondent's score for three and five of the tests, respectively (there was no association with father's education and mother's occupation). After adjustment for the respondent's education, father's occupation was no longer associated with respondent's test score, however, the results were essentially unchanged for mother's education. Conclusions Higher SEP during childhood and greater educational attainment are both associated with cognitive function in adulthood, with mothers and fathers each contributing to their offspring's formative cognitive development and later life cognitive ability (albeit in different ways). Improvements in both parental socioeconomic circumstances and the educational attainment of their offspring could possibly enhance cognitive function and decrease risk of dementia later in life.
Objectives To evaluate whether mid-life marital status is related to cognitive function in later life.Design Prospective population based study with an average follow-up of 21 years.Setting Kuopio ...and Joensuu regions in eastern Finland.Participants Participants were derived from random, population based samples previously investigated in 1972, 1977, 1982, or 1987; 1449 individuals (73%), aged 65-79, underwent re-examination in 1998.Main outcome measures Alzheimer’s disease and mild cognitive impairment.Results People cohabiting with a partner in mid-life (mean age 50.4) were less likely than all other categories (single, separated, or widowed) to show cognitive impairment later in life at ages 65-79. Those widowed or divorced in mid-life and still so at follow-up had three times the risk compared with married or cohabiting people. Those widowed both at mid-life and later life had an odds ratio of 7.67 (1.6 to 40.0) for Alzheimer’s disease compared with married or cohabiting people. The highest increased risk for Alzheimer’s disease was in carriers of the apolipoprotein E e4 allele who lost their partner before mid-life and were still widowed or divorced at follow-up. The progressive entering of several adjustment variables from mid-life did not alter these associations.Conclusions Living in a relationship with a partner might imply cognitive and social challenges that have a protective effect against cognitive impairment later in life, consistent with the brain reserve hypothesis. The specific increased risk for widowed and divorced people compared with single people indicates that other factors are needed to explain parts of the results. A sociogenetic disease model might explain the dramatic increase in risk of Alzheimer’s disease for widowed apolipoprotein E e4 carriers.
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