1.
Sjöberg, Linnea, et al.
(författare)
Prevalence of depression : Comparisons of different depression definitions in population-based samples of older adults
2017
Ingår i: Journal of Affective Disorders. - : Elsevier BV. - 0165-0327 .- 1573-2517. ; 221, s. 123-131
Tidskriftsartikel (refereegranskat) abstract
Background: Depression prevalence in older adults varies largely across studies, which probably reflects methodological rather than true differences. This study aims to explore whether and to what extent the prevalence of depression varies when using different diagnostic criteria and rating scales, and various samples of older adults. Methods: A population-based sample of 3353 individuals aged 60-104 years from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were examined in 2001-2004. Point prevalence of depression was estimated by: 1) diagnostic criteria, ICD-10 and DSM-IV-TR/DSM-5; 2) rating scales, MADRS and GDS-15; and 3) self-report. Depression prevalence in sub-samples by dementia status, living place, and socio-demographics were compared. Results: The prevalence of any depression (including all severity grades) was 4.2% (moderate/severe: 1.6%) for ICD-10 and 9.3% (major: 2.1%) for DSM-IV-TR; 10.6% for MADRS and 9.2% for GDS-15; and 9.1% for selfreport. Depression prevalence was lower in the dementia-free sample as compared to the total population. Furthermore, having poor physical function, or not having a partner were independently associated with higher depression prevalence, across most of the depression definitions. Limitations: The response rate was 73.3% and this may have resulted in an underestimation of depression. Conclusion: Depression prevalence was similar across all depression definitions except for ICD-10, showing much lower figures. However, independent of the definition used, depression prevalence varies greatly by dementia status, physical functioning, and marital status. These findings may be useful for clinicians when assessing depression in older adults and for researchers when exploring and comparing depression prevalence across studies.
2.
Gustavsson, Anders, et al.
(författare)
Cost of disorders of the brain in Europe 2010.
2011
Ingår i: European Neuropsychopharmacology. - Amsterdam : Elsevier BV. - 0924-977X .- 1873-7862. ; 21:10, s. 718-79
Tidskriftsartikel (refereegranskat) abstract
BACKGROUND: The spectrum of disorders of the brain is large, covering hundreds of disorders that are listed in either the mental or neurological disorder chapters of the established international diagnostic classification systems. These disorders have a high prevalence as well as short- and long-term impairments and disabilities. Therefore they are an emotional, financial and social burden to the patients, their families and their social network. In a 2005 landmark study, we estimated for the first time the annual cost of 12 major groups of disorders of the brain in Europe and gave a conservative estimate of €386 billion for the year 2004. This estimate was limited in scope and conservative due to the lack of sufficiently comprehensive epidemiological and/or economic data on several important diagnostic groups. We are now in a position to substantially improve and revise the 2004 estimates. In the present report we cover 19 major groups of disorders, 7 more than previously, of an increased range of age groups and more cost items. We therefore present much improved cost estimates. Our revised estimates also now include the new EU member states, and hence a population of 514 million people.AIMS: To estimate the number of persons with defined disorders of the brain in Europe in 2010, the total cost per person related to each disease in terms of direct and indirect costs, and an estimate of the total cost per disorder and country.METHODS: The best available estimates of the prevalence and cost per person for 19 groups of disorders of the brain (covering well over 100 specific disorders) were identified via a systematic review of the published literature. Together with the twelve disorders included in 2004, the following range of mental and neurologic groups of disorders is covered: addictive disorders, affective disorders, anxiety disorders, brain tumor, childhood and adolescent disorders (developmental disorders), dementia, eating disorders, epilepsy, mental retardation, migraine, multiple sclerosis, neuromuscular disorders, Parkinson's disease, personality disorders, psychotic disorders, sleep disorders, somatoform disorders, stroke, and traumatic brain injury. Epidemiologic panels were charged to complete the literature review for each disorder in order to estimate the 12-month prevalence, and health economic panels were charged to estimate best cost-estimates. A cost model was developed to combine the epidemiologic and economic data and estimate the total cost of each disorder in each of 30 European countries (EU27+Iceland, Norway and Switzerland). The cost model was populated with national statistics from Eurostat to adjust all costs to 2010 values, converting all local currencies to Euro, imputing costs for countries where no data were available, and aggregating country estimates to purchasing power parity adjusted estimates for the total cost of disorders of the brain in Europe 2010.RESULTS: The total cost of disorders of the brain was estimated at €798 billion in 2010. Direct costs constitute the majority of costs (37% direct healthcare costs and 23% direct non-medical costs) whereas the remaining 40% were indirect costs associated with patients' production losses. On average, the estimated cost per person with a disorder of the brain in Europe ranged between €285 for headache and €30,000 for neuromuscular disorders. The European per capita cost of disorders of the brain was €1550 on average but varied by country. The cost (in billion €PPP 2010) of the disorders of the brain included in this study was as follows: addiction: €65.7; anxiety disorders: €74.4; brain tumor: €5.2; child/adolescent disorders: €21.3; dementia: €105.2; eating disorders: €0.8; epilepsy: €13.8; headache: €43.5; mental retardation: €43.3; mood disorders: €113.4; multiple sclerosis: €14.6; neuromuscular disorders: €7.7; Parkinson's disease: €13.9; personality disorders: €27.3; psychotic disorders: €93.9; sleep disorders: €35.4; somatoform disorder: €21.2; stroke: €64.1; traumatic brain injury: €33.0. It should be noted that the revised estimate of those disorders included in the previous 2004 report constituted €477 billion, by and large confirming our previous study results after considering the inflation and population increase since 2004. Further, our results were consistent with administrative data on the health care expenditure in Europe, and comparable to previous studies on the cost of specific disorders in Europe. Our estimates were lower than comparable estimates from the US.DISCUSSION: This study was based on the best currently available data in Europe and our model enabled extrapolation to countries where no data could be found. Still, the scarcity of data is an important source of uncertainty in our estimates and may imply over- or underestimations in some disorders and countries. Even though this review included many disorders, diagnoses, age groups and cost items that were omitted in 2004, there are still remaining disorders that could not be included due to limitations in the available data. We therefore consider our estimate of the total cost of the disorders of the brain in Europe to be conservative. In terms of the health economic burden outlined in this report, disorders of the brain likely constitute the number one economic challenge for European health care, now and in the future. Data presented in this report should be considered by all stakeholder groups, including policy makers, industry and patient advocacy groups, to reconsider the current science, research and public health agenda and define a coordinated plan of action of various levels to address the associated challenges.RECOMMENDATIONS: Political action is required in light of the present high cost of disorders of the brain. Funding of brain research must be increased; care for patients with brain disorders as well as teaching at medical schools and other health related educations must be quantitatively and qualitatively improved, including psychological treatments. The current move of the pharmaceutical industry away from brain related indications must be halted and reversed. Continued research into the cost of the many disorders not included in the present study is warranted. It is essential that not only the EU but also the national governments forcefully support these initiatives.
3.
Imahori, Yume, et al.
(författare)
Association of ischemic heart disease with long-term risk of cognitive decline and dementia : A cohort study
2023
Ingår i: Alzheimer's & Dementia. - 1552-5260 .- 1552-5279. ; 19:12, s. 5541-5549
Tidskriftsartikel (refereegranskat) abstract
INTRODUCTION: The independent and joint effect of ischemic heart disease (IHD) and coexisting atrial fibrillation (AF) and heart failure (HF) on dementia risk is largely unknown.METHODS: This population-based cohort study included 2568 dementia-free participants (age ≥60 years) in SNAC-K, who were regularly examined from 2001–2004 through 2013–2016. Dementia was diagnosed following the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria. Global cognitive function was assessed using a global cognitive composite z-score derived from five cognitive domains. Data were analyzed using Cox, Fine-Gray, and linear mixed-effects models.RESULTS: Overall, IHD at baseline was associated with multivariable-adjusted hazard ratio (HR) of 1.39 (95% confidence interval = 1.06−1.82) for dementia and multivariable-adjusted β-coefficient of −0.02 (−0.03 to −0.01) for annual changes in global cognitive z-score, independent of AF, HF, and cerebrovascular disease. Coexisting AF or HF did not add further risk to dementia and cognitive decline.DISCUSSION: IHD is independently associated with dementia and cognitive decline in older adults, whereas coexisting AF/HF is not associated with an increased risk.
4.
Laukka, Erika J., et al.
(författare)
Combined Genetic Influences on Episodic Memory Decline in Older Adults Without Dementia
2020
Ingår i: Neuropsychology. - : American Psychological Association (APA). - 0894-4105 .- 1931-1559. ; 34:6, s. 654-666
Tidskriftsartikel (refereegranskat) abstract
Objective: Although heritability explains a large proportion of the variance in old-age cognition, studies on the influence of specific genes have been inconclusive. We investigated the individual and combined effects of four single polymorphisms, previously associated with episodic memory, on cognitive or performance and rate of change. Method: Participants were 2490 individuals without dementia (mean age = 72 years) from the population-based Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). Genotyping was performed for APOE (rs429358, rs7412), BDNF (rs6265), KIBRA (rs17070145), and CLSTN2 (rs6439886). We used latent difference score models to estimate the effects of age and genetic variation on level and change in five latent cognitive factors: episodic and semantic memory, letter and category fluency, and perceptual speed. Results: Of the individual genes, only APOE was associated with cognitive performance; epsilon 4 carriers showed lower perceptual speed performance and faster category fluency decline. A cumulative score, combining APOE, BDNF, KIBRA and CLSTN2, was associated with faster cognitive decline that was specific to the episodic memory domain (regression coefficient -0.064, p < .01). Similar results were obtained for a score not including APOE. Conclusions: Results suggest a benefit of investigating the combined influence of polymorphisms related to specific mechanistic factors.
5.
Papenberg, Goran, et al.
(författare)
Anticholinergic drug use is associated with episodic memory decline in older adults without dementia
2017
Ingår i: Neurobiology of Aging. - : Elsevier BV. - 0197-4580 .- 1558-1497. ; 55, s. 27-32
Tidskriftsartikel (refereegranskat) abstract
Anticholinergic drug use is common in older adults and has been related to increased dementia risk. This suggests that users of these drugs may experience accelerated cognitive decline. So far, however, longitudinal data on this topic are absent and the available evidence is inconclusive with respect to effects on specific cognitive domains due to suboptimal control of confounding variables. We investigated whether anticholinergic medication use is associated with cognitive decline over 6 years in a population-based study of older adults (aged 60-90; n = 1473) without dementia. We found that users (n = 29) declined more on episodic memory over 6 years compared to nonusers (n = 1418). These results were independent of age, sex, education, overall drug intake, physical activity, depression, cardiovascular risk burden, and cardiovascular disease. By contrast, anticholinergic drug use was unrelated to performance in processing speed, semantic memory, short-term memory, verbal fluency, and global cognition (the Mini-Mental-State Examination). Our results suggest that effects of anticholinergics may be particularly detrimental to episodic memory in older adults, which supports the assertion that the cholinergic system plays an important role in episodic memory formation.
6.
Papenberg, Goran, et al.
(författare)
Magnified effects of the COMT gene on white-matter microstructure in very old age
2015
Ingår i: Brain Structure and Function. - : Springer Science and Business Media LLC. - 1863-2653 .- 1863-2661. ; 220:5, s. 2927-2938
Tidskriftsartikel (refereegranskat) abstract
Genetic factors may partly account for between-person differences in brain integrity in old age. Evidence from human and animal studies suggests that the dopaminergic system is implicated in the modulation of white-matter integrity. We investigated whether a genetic variation in the Catechol-O-Methyltransferase (COMT) Val158Met polymorphism, which influences dopamine availability in prefrontal cortex, contributes to interindividual differences in white-matter microstructure, as measured with diffusion-tensor imaging. In a sample of older adults from a population-based study (60-87 years; n = 238), we found that the COMT polymorphism affects white-matter microstructure, indexed by fractional anisotropy and mean diffusivity, of several white-matter tracts in the oldest age group (81-87 years), although there were no reliable associations between COMT and white-matter microstructure in the two younger age groups (60-66 and 72-78 years). These findings extend previous observations of magnified genetic effects on cognition in old age to white-matter integrity.
7.
Speh, Andreja, et al.
(författare)
Cardiovascular Health and Rate of Cognitive Decline in Preclinical Dementia : A 12-Year Population-Based Study
2024
Ingår i: Neuropsychology. - 0894-4105 .- 1931-1559. ; 38:3, s. 211-222
Tidskriftsartikel (refereegranskat) abstract
Objective: We investigated whether vascular risk factors (VRFs), assessed with Life’s Simple 7 (LS7), are associated with the rate of cognitive decline in the years preceding a dementia diagnosis. Method: This study included 1,449 stroke-free participants aged ≥60 years from the Swedish National Study on Aging and Care in Kungsholmen, who underwent repeated neuropsychological testing (episodic memory, semantic memory, verbal fluency, perceptual speed) across 12 years. The LS7 score, assessed at baseline, included smoking, diet, physical activity, body mass index, plasma glucose, total cholesterol, and blood pressure. Preclinical dementia was defined as being dementia-free at baseline and diagnosed with dementia during follow-up. Level and change in cognitive performance as a function of LS7 category (poor vs. intermediate to optimal) and future dementia status were estimated using linear mixed-effect models. Results: Participants who later developed dementia had, on average, a poorer LS7 score compared to those who remained dementia-free. For individuals aged 60–72 years, poor diet was associated with accelerated decline in perceptual speed (β = −0.05, 95% CI [−0.08, −0.02]), and a poor glucose score was associated with faster rates of verbal fluency (β = −0.019, 95% CI [−0.09, −0.01]) and global cognitive (β = −0.028, 95% CI [−0.06, 0.00]) decline in the preclinical dementia group. Conclusions: VRFs exacerbate rate of cognitive decline in the years preceding a dementia diagnosis. This effect was most pronounced in young–old age and primarily driven by diet and glucose. The effect of VRFs may be especially detrimental for cognitive decline trajectories of individuals with impending dementia.
8.
Wang, Rui, et al.
(författare)
MRI load of cerebral microvascular lesions and neurodegeneration, cognitive decline, and dementia
2018
Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 91:16, s. 1487-1497
Tidskriftsartikel (refereegranskat) abstract
Objective To explore the differential associations of neurodegeneration and microvascular lesion load with cognitive decline and dementia in older people and the modifying effect of the APOE genotype on these associations. Methods A sample of 436 participants (age >= 60 years) was derived from the population-based Swedish National study on Aging and Care in Kungsholmen, Stockholm, and clinically examined at baseline (2001-2003) and 3 occasions during the 9-year follow-up. At baseline, we assessed microvascular lesion load using a summary score for MRI markers of lacunes, white matter hyperintensities (WMHs), and perivascular spaces and neurodegeneration load for markers of enlarged ventricles, smaller hippocampus, and smaller gray matter. We assessed cognitive function using the Mini-Mental State Examination (MMSE) test and diagnosed dementia following the Diagnostic and Statistical Manual of Mental Disorders, 4th edition criteria. We analyzed data using linear mixed-effects, mediation, and random-effects Cox models. Results During the follow-up, 46 participants were diagnosed with dementia. Per 1-point increase in microvascular lesion and neurodegeneration score (range 0-3) was associated with multiple adjusted beta-coefficients of -0.35 (95% confidence interval, -0.51 to -0.20) and -0.44 (-0.56 to -0.32), respectively, for the MMSE score and multiple adjusted hazard ratios of 1.68 (1.12-2.51) and 2.35 (1.58-3.52), respectively, for dementia; carrying APOE epsilon 4 reinforced the associations with MMSE decline. WMH volume changes during the follow-up mediated 66.9% and 12.7% of the total association of MMSE decline with the baseline microvascular score and neurodegeneration score, respectively. Conclusions Both cerebral microvascular lesion and neurodegeneration loads are strongly associated with cognitive decline and dementia. The cognitive decline due to microvascular lesions is exacerbated by APOE epsilon 4 and is largely attributed to progression and development of microvascular lesions.
9.
Xu, Wei-Li, et al.
(författare)
Accelerated Progression from Mild Cognitive Impairment to Dementia Among APOE epsilon 4 epsilon 4 Carriers
2013
Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 33:2, s. 507-515
Tidskriftsartikel (refereegranskat) abstract
The impact of APOE ε4 on mild cognitive impairment (MCI) and its progression to dementia remain controversial. We aimed to examine the association of APOE ε4 with MCI, and to verify the hypothesis that ε4 accelerates progression from MCI to dementia. In the Kungsholmen project, 756 cognitively healthy participants and 212 people with MCI aged ≥75 years were identified at baseline. Amnestic MCI (aMCI) and other cognitive impairment no dementia (oCIND) as two subtypes of MCI were assessed based on standard definitions. The two cohorts were followed for 9 years to detect incident cases of MCI and dementia following international criteria. APOE genotypes were assessed at baseline. Data were analyzed using Cox models. During the follow-up, in the cognitively healthy cohort, 165 people developed MCI (40 aMCI and 125 oCIND) and 176 developed dementia; in the MCI cohort, 118 persons progressed to dementia. Compared with APOE ε3ε3, the hazard ratios (HRs) (95% CIs) of ε2ε4/ε3ε4 were 2.24 (1.10-4.57) for aMCI and 1.78 (1.15-2.75) for oCIND, while the ε4ε4 was related to dementia with a HR of 4.35 (1.97-9.63) in the cognitively healthy cohort. In the MCI cohort, the ε4ε4 genotype led to a multi-adjusted HR of 2.89 (1.12-7.48) for dementia and accelerated the progression to dementia by 3.36 years. The APOE ε4 heterozygotes are associated with an increased risk of aMCI and oCIND. The ε4 homozygote substantially accelerates progression from MCI to dementia, and anticipate dementia occurrence by more than 3 years in people with MCI.
10.
Caracciolo, Barbara, et al.
(författare)
Relationship of Subjective Cognitive Impairment and Cognitive Impairment No Dementia to Chronic Disease and Multimorbidity in a Nation-Wide Twin Study
2013
Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 36:2, s. 275-284
Tidskriftsartikel (refereegranskat) abstract
We investigated the relation of subjective cognitive impairment (SCI) and cognitive impairment no dementia (CIND) to common chronic diseases of the elderly and multimorbidity, and assessed the contribution of genetic background and shared familial environment to these associations. Subjects were 11,379 dementia-free twin individuals aged >= 65 from the Swedish Twin Registry. SCI was defined as subjective complaint of cognitive change without objective cognitive impairment and CIND was defined according to current criteria. In unmatched, fully-adjusted regression models, mental, musculoskeletal, respiratory, and urological diseases were all significantly associated with increased odds ratios (ORs) of SCI and CIND. Circulatory and gastrointestinal diseases were related to SCI only, while endocrine diseases were associated with CIND. The adjusted ORs of multimorbidity were 2.1 [95% confidence intervals (95% CI): 1.8-2.3] for SCI and 1.5 for CIND (95% CI: 1.3-1.8). A dose-dependent relationship was observed between number of chronic diseases and ORs for SCI but not for CIND. In co-twin control analyses, the chronic diseases-SCI association was largely unchanged. On the other hand, the chronic diseases-CIND association was no longer statistically significant, except for cancer, where an increased OR was observed. In conclusion, chronic morbidity is associated with both SCI and CIND but disease profiles do not always overlap between the two cognitive syndromes. The association is stronger when diseases co-occur, especially for SCI. Genetic and early-life environmental factors may partially explain the association of CIND but not that of SCI with chronic diseases.
