OBJECTIVE: To investigate the longitudinal relationship between body mass index (BMI), a major vascular risk factor, and cerebral atrophy, a marker of neurodegeneration, in a population-based sample of middle-aged women. METHODS: A representative sample of 290 women born in 1908, 1914, 1918, and 1922 was examined in 1968 to 1969, 1974 to 1975, 1980 to 1981, and 1992 to 1993 as part of the Population Study of Women in Göteborg, Sweden. At each examination, women completed a survey on a variety of health and lifestyle factors and underwent anthropometric, clinical, and neuropsychiatric assessments and blood collection. Atrophy of the temporal, frontal, occipital, and parietal lobes was measured on CT in 1992 when participants were age 70 to 84. Univariate and multivariate regression analyses were used to assess the relationship between BMI and brain measures. RESULTS: Women with atrophy of the temporal lobe were, on average, 1.1 to 1.5 kg/m2 higher in BMI at all examinations than women without temporal atrophy (p
Comment In: Neurology. 2005 Jun 14;64(11):1990-1; author reply 1990-115955971
SummaryForPatientsIn: Neurology. 2004 Nov 23;63(10):E19-2015557485
Overweight and obesity in mid- and late-life may increase risk for dementia, whereas a decline in body weight or body mass index (BMI) and underweight in years preceding a clinical dementia diagnosis are also associated with dementia. Little is known about the modifying effect of the APOE genotype, a major susceptibility gene for Alzheimer's disease (AD), on the BMI-dementia adult life course trajectory.
We evaluated the exposure, BMI, in relationship to the outcome, clinical dementia, over 37 years, considering the effect modification of the APOE ?4 allele.
The Prospective Population Study of Women (PPSW) in Sweden is a systematic sample of 1462 women born 1908, 1914, 1918, 1922, and 1930 and aged 38-60 years at baseline. Examinations occurred in 1968, 1974, 1980, 1992, 2000, and 2005; 559 women had information on dementia, BMI, and APOE ?4 allele status, in addition to covariates. Statistical analyses were conducted using mixed effects regression models.
Trajectories of BMI over 37 years differed by APOE ?4 allele status. While women gained BMI similarly from mid-life to age 70 years, women with at least one APOE ?4 allele experienced BMI decline more quickly after age 70 years compared to women without an APOE ?4 allele. However, upon stratifying the sample by dementia occurrence, it appeared that dementia drove the overall BMI-trajectory. There was a main effect of age, interactions of age by APOE ?4 allele status, and age by presence versus absence of dementia.
Women with similar average BMI at mid-life exhibited different BMI trajectories in relation to dementia occurrence. In addition, the pattern of BMI decline in late-life differed on the basis of APOE ?4 allele possession. Thus, these data suggest roles for both dementia- and APOE-associated changes in BMI during the adult life course.
Level of adiposity is linked to dementia in epidemiological studies. Overweight and obesity in mid- and late-life may increase risk for dementia, whereas decline in body weight or body mass index (BMI) and underweight in years preceding and at the time of a dementia diagnosis may also relate to dementia. Longitudinal studies with sufficient follow-up are necessary to estimate trajectories that allow better understanding of the relationship between adiposity indices and dementia over the life course. We evaluated the natural history of BMI in relationship to clinical dementia over 37 years in the Prospective Population Study of Women (PPSW) in Sweden. PPSW is a systematic sample of 1462 women born 1908, 1914, 1918, 1922, and 1930 and aged 38-60 years at baseline. Examinations occurred in 1968, 1974, 1980, 1992, 2000, and 2005. Statistical analyses were conducted using mixed effects regression models. Trajectories of BMI over 37 years as a function of age differed between women who did versus did not develop dementia. Women developing dementia evidenced a lesser increase in BMI from age 38 to 70 years. After age 70, the BMI slope decreased similarly (no "accelerated decline") irrespective of dementia status. A lower BMI before and during dementia onset was observed. Women with similar BMI at mid-life exhibited a different pattern of BMI change as they approached late-life that was related to dementia onset. BMI may be a potential marker of dementia-related neuropathologies in the brain. Dementia is related to a common risk factor, BMI, from mid-to late-life.
Dementia includes a group of neuro-degenerative disorders characterized by varying degrees of cognitive impairment. Recent data indicates that blood group AB is associated with impaired cognition in elderly patients. To date there are no large-scale studies that have examined the relationship between ABO blood group and dementia-related disorders in detail.
We used data from the SCANDAT2 database that contains information on over 1.6 million blood donors from 1968 in Sweden and 1981 from Denmark. The database was linked with health outcomes data from nationwide patient and cause of death registers to investigate the relationship between blood groups and risk of different types of dementia. The incident rate ratios were estimated using log-linear Poisson regression models.
Among 1,598,294 donors followed over 24 million person-years of observation we ascertained 3,615 cases of Alzheimer's disease, 1,842 cases of vascular dementia, and 9,091 cases of unspecified dementia. Overall, our study showed no association between ABO blood group and risk of Alzheimer's disease, vascular dementia or unspecified dementia. This was also true when analyses were restricted to donors aged 70 years or older except for a slight, but significantly decreased risk of all dementia combined in subjects with blood group A (IRR, 0.93; 95% confidence interval [CI], 0.88-0.98), compared to those with blood group O.
Our results provide no evidence that ABO blood group influences the risk of dementia.
AIM: Using the unique Danish psychiatric and somatic health registers, we investigated the rate of subsequent dementia in patients with late-onset acute and transient psychosis. METHODS: By linkage of the psychiatric and the somatic nationwide registers of all patients with in- or outpatient hospital contact in Denmark, we included all patients with a first ever contact during the period 1 January 1994 to 31 December 2001 with one of the main index diagnoses: late-onset acute and transient psychosis or osteoarthritis. Data on the general population were also included. The first diagnosis of dementia for each individual at discharge or at outpatient contact was established. Poisson regression models were used to compare the cohorts of patients with dementia as the outcome of interest. RESULTS: Using a cut-off age of 60 years, 8062 individuals were included. Significant associations were found between a subsequent diagnosis of dementia and the index diagnosis, age and calendar time. Overall, the rate ratio for developing dementia in late-onset acute and transient psychosis compared to osteoarthritis patients was 10.86 (95% confidence intervals, 8.42 and 14.00, respectively), however, the magnitude of the rate ratio varied according to sex, age, duration since diagnosis and calendar time. Compared to the general population, the rate ratio was 8.12 (95% confidence intervals, 6.77 and 9.74, respectively). CONCLUSION: The present study has established that subjects with late-onset acute and transient psychosis are at 11 times higher risk of subsequently getting a diagnosis of dementia compared to patients with osteoarthritis, and at 8 times higher risk compared to the general population.
An inverse relationship between educational level and dementia has been reported in several studies. In this study we investigated the relationship between educational level and dementia related deaths for cohorts of people all born during 1915-39. The cohorts were followed up from adulthood or old age, taking into account possible confounders and mediating paths. Our study population comprised participants in Norwegian health examination studies in the period 1974-2002; The Counties Study and Cohort of Norway (CONOR). Dementia related deaths were defined as deaths with a dementia diagnosis on the death certificate and linked using the Cause of Death Registry to year 2012. The study included 90,843 participants, 2.06 million person years and 2440 dementia related deaths. Cox regression was used to assess the association between education and dementia related deaths. Both high and middle educational levels were associated with lower dementia related death risk compared to those with low education when follow-up started in adulthood (35-49 years, high versus low education: HR=0.68, 95% confidence interval (CI) 0.50-0.93; 50-69 years, high versus low education: HR=0.52, 95% CI 0.34-0.80). However, when follow-up started at old age (70-80 years) there was no significant association between education and dementia related death. Restricting the study population to those born during a five-year period 1925-29 (the birth cohort overlapping all three age groups), gave similar main findings. The protective effects found for both high and middle educational level compared to low education were robust to adjustment for cardiovascular health and life style factors, suggesting education to be a protective factor for dementia related death. Both high and middle educational levels were associated with decreased dementia related death risk compared with low educational level when follow-up started in adulthood, but no association was observed when follow-up started at old age.
In anticipation of the sequencing of the human genome and description of the human proteome, the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik) was initiated in 2002. AGES-Reykjavik was designed to examine risk factors, including genetic susceptibility and gene/environment interaction, in relation to disease and disability in old age. The study is multidisciplinary, providing detailed phenotypes related to the cardiovascular, neurocognitive (including sensory), and musculoskeletal systems, and to body composition and metabolic regulation. Relevant quantitative traits, subclinical indicators of disease, and medical diagnoses are identified by using biomarkers, imaging, and other physiologic indicators. The AGES-Reykjavik sample is drawn from an established population-based cohort, the Reykjavik Study. This cohort of men and women born between 1907 and 1935 has been followed in Iceland since 1967 by the Icelandic Heart Association. The AGES-Reykjavik cohort, with cardiovascular risk factor assessments earlier in life and detailed late-life phenotypes of quantitative traits, will create a comprehensive study of aging nested in a relatively genetically homogeneous older population. This approach should facilitate identification of genetic factors that contribute to healthy aging as well as the chronic conditions common in old age.
CONTEXT: In spite of numerous studies on the occurrence of dementia, many questions remain, such as the relation between age, aging, and dementing disorders. This question is relevant both for understanding the pathogenetic mechanism of the dementias and for the public health prospective because of the increasing number of 85-year-old or older persons in our population. OBJECTIVE: To estimate the occurrence of dementia in the very old, including nonagenarians, in relation to age, gender, and different dementia types. DESIGN: An epidemiological survey where all participants were clinically examined by physicians, assessed by psychologists, and interviewed by nurses. The Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) criteria for dementia were followed. A category of "questionable dementia" was added when all criteria were not fulfilled. A double diagnostic procedure was used for all subjects. SETTING: Community-based population, including all inhabitants of 2 areas in central Stockholm, Sweden (N = 1848). PARTICIPANTS: Of the 1848 subjects in the study population, 168 (9.1%) had died and 56 (3%) moved before examination. Of the remaining subjects, 1424 (87.7%) were examined, and the refusal rate was 12.3%. MAIN OUTCOME MEASURES: Age- and gender-specific prevalence figures, and gender- and education-adjusted odds ratios were used. RESULTS: At the end of the diagnostic procedure, 358 clinically definite cases of dementia and 101 questionable cases of dementia were identified. Alzheimer disease (AD) contributed to 76.5%, and vascular dementia (VaD) to 17.9%. The prevalence of dementia increases from 13% in the 77- to 84-year-old subjects to 48% among persons 95 years and older (from 18% to 61% when questionable cases were included). The odds ratio for subjects 90 to 94 years and 95 years and older in comparison with 77- to 84-year-old subjects was 3.7 (95% confidence interval [CI], 2.7-5.1) and 6.5 (95% CI, 3.9-10.8) for dementia, 4.8 (95% CI, 3.3-7.0) and 8.0 (95% CI, 4.6-14.0) for persons with AD, 2.3 (95% CI, 1.3-4.2) and 4.6 (95% CI, 1.9-11.2) for VaD, respectively. CONCLUSIONS: Dementia prevalence continues to increase even in the most advanced ages. This increase is especially evident among women and is more clear for AD. We believe that our prevalence data reflect the differential distribution of dementia risk.
Aging Research Center, Division of Geriatric Epidemiology and Medicine, Department of Neurotec, Karolinska Institutet and the Stockholm Gerontology Research Center, Olivecronas väg 4, Box 6401, S-113 82 Stockholm, Sweden.
To explore the relationship between light to moderate alcohol consumption and risk of dementia and Alzheimer's disease in very old people, a community-based dementia-free cohort (n = 402) was followed for almost 6 years to detect incident dementia using the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition-Revised criteria. Data from the entire cohort and a subpopulation of those with baseline Mini-Mental State Examination score > or =24 (n = 317) were analyzed with Cox models. In the entire population, light to moderate drinking was significantly associated with a decreased risk of incident dementia and Alzheimer's disease compared with nondrinking (adjusted relative risk 0.5, 95% confidence interval 0.3 to 0.7). In the analysis of the subpopulation, however, the inverse association between light to moderate drinking and risk of incident dementia and Alzheimer's disease was less evident and no longer statistically significant. This study suggested that light to moderate alcohol drinking might protect against dementia and Alzheimer's disease among old people, although the possibility that such an association may be due to information bias cannot be totally ruled out.