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Sökning: L773:1420 8008 OR L773:1421 9824 > Kivipelto M

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1.
  • Aguero-Torres, H, et al. (författare)
  • Rethinking the dementia diagnoses in a population-based study : What is Alzheimer's disease and what is vascular dementia? A study from the Kungsholmen Project
  • 2006
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - Basel : Karger. - 1420-8008 .- 1421-9824. ; 22:3, s. 244-249
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To explore the hypothesis that older adults often are affected by more than one disease, making the differential diagnosis between Alzheimer’s disease (AD) and vascular dementia (VaD) difficult. Methods: Incident dementia cases (n = 308) from a population-based longitudinal study of people 75+ years were investigated. The DSM-III-R criteria were used for the clinical diagnosis of dementia. Data on vascular disorders (hypertension, cerebrovascular and ischemic heart diseases, heart failure, atrial fibrillation, diabetes) as well as type of onset/course of dementia were used retrospectively to reclassify dementias. Results: Only 47% of the AD cases were reclassified as pure AD without any vascular disorder. Among subjects with AD and with a vascular component, cerebrovascular disease was the most common (41%). Only 25% of VaD were reclassified as pure VaD. Further, 26% of the pure AD subjects developed a vascular disorder in the following 3 years. Conclusions: Both vascular and degenerative mechanisms may often contribute to the expression of dementia among the elderly. Most of the AD cases have vascular involvements, and pure dementia types in very old subjects constitute only a minority of dementia cases.
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2.
  • Alenius, M, et al. (författare)
  • Education-Based Cutoffs for Cognitive Screening of Alzheimer's Disease
  • 2022
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 51:1, s. 42-55
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Introduction:</i></b> The educational background and size of the elderly population are undergoing significant changes in Finland during the 2020s. A similar process is likely to occur also in several European countries. For cognitive screening of early Alzheimer’s disease (AD), using outdated norms and cutoff scores may negatively affect clinical accuracy. The aim of the present study was to examine the effects of education, age, and gender on the Consortium to Establish a Registry for Alzheimer’s Disease neuropsychological battery (CERAD-nb) in a large register-based, clinical sample of patients with mild AD and nondemented at-risk persons from the general population (controls) and to examine whether corrected cutoff scores would increase the accuracy of differentiation between the 2 groups. <b><i>Methods:</i></b> CERAD-nb scores were obtained from AD patients (<i>n</i> = 389, 58% women, mean age 74.0 years) and from controls (<i>n</i> = 1,980, 52% women, mean age 68.5 years). The differences in CERAD-nb performance were evaluated by univariate GLM. Differentiation between the 2 groups was evaluated using a receiver operating characteristic (ROC) curve, where a larger area under the ROC curve represents better discrimination. Youden’s J was calculated for the overall performance and accuracy of each of the measures. <b><i>Results:</i></b> Of the demographic factors, education was the strongest predictor of CERAD-nb performance, explaining more variation than age or gender in both the AD patients and the controls. Education corrected cutoff scores had better diagnostic accuracy in discriminating between the AD patients and controls than existing uncorrected scores. The highest level of discrimination between the 2 groups overall was found for two CERAD-nb total scores. <b><i>Conclusions:</i></b> Education-corrected cutoff scores were superior to uncorrected scores in differentiating between controls and AD patients especially for the highest level of education and should therefore be used in clinical cognitive screening, also as the proportion of the educated elderly is increasing substantially during the 2020s. Our results also indicate that total scores of the CERAD-nb are better at discriminating AD patients from controls than any single subtest score. A digital tool for calculating the total scores and comparing education-based cutoffs would increase the efficiency and usability of the test.
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3.
  • Annerbo, S, et al. (författare)
  • A prospective study on the development of Alzheimer's disease with regard to thyroid-stimulating hormone and homocysteine
  • 2009
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 28:3, s. 275-280
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background/Aim: </i>The combination of elevated total homocysteine (tHcy) levels and low levels of thyroid-stimulating hormone (TSH) are linked to Alzheimer’s disease (AD) in some studies, although the evidence is mixed. Our objective was to prospectively investigate the association between tHcy and TSH and the subsequent development of AD. <i>Methods:</i> A subsample of 200 nondemented subjects was taken from the Kungsholmen Project, a population-based study among people ≥75 years. Information about tHcy and TSH levels were taken from the baseline investigation of the Kungsholmen Project study. <i>Results: </i>Increased tHcy levels were related to an elevated risk of AD (n = 61) after a mean follow-up time of 6.7 years. People with high tHcy (the 3rd tertile) had more than twice as high a risk of developing AD than those with low tHcy, even after adjusting for age, sex, education, ApoE status, MMSE score and laboratory parameters. tHcy was negatively correlated with TSH (p = 0.02). There was neither an influence of TSH nor an interaction between tHcy and TSH in the development of AD. <i>Conclusions: </i>These results suggest that homocysteine, but not TSH, is involved in the development of AD. The connection between elevated tHcy and low TSH levels needs to be studied further.
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4.
  • Julkunen, V, et al. (författare)
  • Cortical thickness analysis to detect progressive mild cognitive impairment: a reference to Alzheimer's disease
  • 2009
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 28:5, s. 404-412
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background/Aims:</i> Mild cognitive impairment (MCI) is associated with an increased risk of Alzheimer’s disease (AD). It would be advantageous to be able to distinguish the characteristics of those MCI patients with a high probability to progress to AD if one wishes to monitor the disease development and treatment. <i>Methods:</i> We assessed the baseline MRI and maximum of 7 years clinical follow-up data of 60 MCI subjects in order to examine differences in cortical thickness (CTH) between the progressive MCI (P-MCI) and stable MCI (S-MCI) subjects. CTH was measured using an automatic computational surface-based method. During the follow-up, 15 MCI subjects converted to AD on average 1.9 ± 1.3 years after the baseline examination, while 45 MCI subjects remained stable. <i>Results:</i> The P-MCI group displayed significantly reduced CTH bilaterally in the superior and middle frontal, superior, middle and inferior temporal, fusiform and parahippocampal regions as well as the cingulate and retrosplenial cortices and also in the right precuneal and paracentral regions compared to S-MCI subjects. <i>Conclusions:</i> Analysis of CTH could be used in conjunction with neuropsychological testing to identify those subjects with imminent conversion from MCI to AD several years before dementia diagnosis.
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5.
  • Komulainen, P, et al. (författare)
  • Metabolic syndrome and cognitive function: a population-based follow-up study in elderly women
  • 2007
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 23:1, s. 29-34
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Objective:</i> To test the hypothesis that metabolic syndrome predicts cognitive impairment, and to examine the association of single metabolic risk factors with cognitive functioning. <i>Methods:</i> Weperformed a 12-year follow-up study in a population-based sample of 101 women aged 60–70 years at baseline. Metabolic syndrome wasdefined by the National Cholesterol Education Program criteria (≧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. <i>Results:</i> 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. <i>Conclusion:</i> In elderly women, metabolic syndrome may be an important contributor to worsening of memory, which is an essential part of mild cognitive impairment.
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6.
  • Laitinen, MH, et al. (författare)
  • Fat intake at midlife and risk of dementia and Alzheimer's disease: a population-based study
  • 2006
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 22:1, s. 99-107
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background:</i> Lifestyle and vascular factors have been linked to dementia and Alzheimer’s disease (AD), but the role of dietary fats in the development of dementia is less clear. <i>Methods:</i> Participants were derived from random, population-based samples initially studied in midlife (1972, 1977, 1982, or 1987). Fat intake from spreads and milk products was assessed using a structured questionnaire and an interview. After an average follow-up of 21 years, a total of 1,449 (73%) individuals aged 65–80 years participated in the re-examination in 1998. Altogether 117 persons had dementia. <i>Results: </i>Moderate intake of polyunsaturated fats at midlife decreased the risk of dementia even after adjustment for demographic variables, other subtypes of fats, vascular risk factors and disorders, and apolipoprotein E (ApoE) genotype (OR 0.40, CI 0.17–0.94 for the 2nd quartile vs. 1st quartile), whereas saturated fat intake was associated with an increased risk (OR 2.45, CI 1.10–5.47 for the 2nd quartile). The associations were seen only among the ApoE &#917;4 carriers. <i>Conclusions:</i> Moderate intake of unsaturated fats at midlife is protective, whereas a moderate intake of saturated fats may increase the risk of dementia and AD, especially among ApoE &#917;4 carriers. Thus, dietary interventions may potentially modify the risk of dementia, particularly among genetically susceptible individuals.
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7.
  • Ngandu, T, et al. (författare)
  • Alcohol drinking and cognitive functions: findings from the Cardiovascular Risk Factors Aging and Dementia (CAIDE) Study
  • 2007
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 23:3, s. 140-149
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background:</i> Moderate alcohol drinking is suggested to be beneficial for cognitive functions, but the results of previous studies have varied greatly. Little is known about the effects of midlife alcohol drinking on the cognitive functions later in life. <i>Methods:</i> Participants were derived from random, population-based samples studied in Eastern Finland in 1972, 1977, 1982, or 1987. A total of 1,341 participants were reexamined in 1998, after an average follow-up period of 21 years, at ages 65–79 years. <i>Results:</i> The participants who did not drink alcohol at midlife had a poorer performance in episodic memory, psychomotor speed, and executive function in late life as compared with infrequent and frequent drinkers, adjusted for sociodemographic and vascular factors. Also late-life nondrinkers had poorer psychomotor speed and executive function. These findings were evident especially among nonsmokers. Further, no interactions between apolipoprotein E4 and alcohol or sex and alcohol were found. <i>Conclusions:</i> Alcohol drinking both at midlife and later is favorably related to the function in several cognitive domains, including episodic memory, psychomotor speed, and executive function, in late life. However, it is not clear whether the association is causal, what is the possible mechanism, and what would be a safe limit of drinking for the best cognitive function.
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8.
  • Olazaran, J, et al. (författare)
  • Nonpharmacological therapies in Alzheimer's disease: a systematic review of efficacy
  • 2010
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 30:2, s. 161-178
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Introduction:</i> Nonpharmacological therapies (NPTs) can improve the quality of life (QoL) of people with Alzheimer’s disease (AD) and their carers. The objective of this study was to evaluate the best evidence on the effects of NPTs in AD and related disorders (ADRD) by performing a systematic review and meta-analysis of the entire field. <i>Methods:</i> Existing reviews and major electronic databases were searched for randomized controlled trials (RCTs). The deadline for study inclusion was September 15, 2008. Intervention categories and outcome domains were predefined by consensus. Two researchers working together detected 1,313 candidate studies of which 179 RCTs belonging to 26 intervention categories were selected. Cognitive deterioration had to be documented in all participants, and degenerative etiology (indicating dementia) had to be present or presumed in at least 80% of the subjects. Evidence tables, meta-analysis and summaries of results were elaborated by the first author and reviewed by author subgroups. Methods for rating level of evidence and grading practice recommendations were adapted from the Oxford Center for Evidence-Based Medicine. <i>Results:</i> Grade A treatment recommendation was achieved for institutionalization delay (multicomponent interventions for the caregiver, CG). Grade B recommendation was reached for the person with dementia (PWD) for: improvement in cognition (cognitive training, cognitive stimulation, multicomponent interventions for the PWD); activities of daily living (ADL) (ADL training, multicomponent interventions for the PWD); behavior (cognitive stimulation, multicomponent interventions for the PWD, behavioral interventions, professional CG training); mood (multicomponent interventions for the PWD); QoL (multicomponent interventions for PWD and CG) and restraint prevention (professional CG training); for the CG, grade B was also reached for: CG mood (CG education, CG support, multicomponent interventions for the CG); CG psychological well-being (cognitive stimulation, multicomponent interventions for the CG); CG QoL (multicomponent interventions for PWD and CG). <i>Conclusion:</i> NPTs emerge as a useful, versatile and potentially cost-effective approach to improve outcomes and QoL in ADRD for both the PWD and CG.
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9.
  • Pennanen, C, et al. (författare)
  • The effect of apolipoprotein polymorphism on brain in mild cognitive impairment: a voxel-based morphometric study
  • 2006
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 22:1, s. 60-66
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the effect of apolipoprotein E (ApoE) on the whole brain in 51 individuals with mild cognitive impairment using voxel-based morphometry. Between cases heterozygous for the ApoE &#917;4 (n = 15) and those who were ApoE &#917;4 noncarriers (n = 28), only the right parahippocampal gyrus, with the entorhinal cortex included, reached the level of statistical significance. In cases homozygous for the &#917;4 allele (n = 8) versus noncarriers, the greatest atrophy was located in the right amygdala followed by the right parahippocampal gyrus, the left amygdala and the left medial dorsal thalamic nucleus.
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10.
  • Rusanen, M, et al. (författare)
  • Midlife smoking, apolipoprotein E and risk of dementia and Alzheimer's disease : a population-based cardiovascular risk factors, aging and dementia study
  • 2010
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 30:3, s. 277-284
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To elucidate the effect of midlife smoking on the risk of dementia and Alzheimer's disease (AD), and the possible modification of this relation by the apolipoprotein E (APOE) ε4.METHODS: Participants of the Cardiovascular Risk Factors, Aging and Dementia study were randomly selected from population-based samples originally studied in midlife (1972, 1977, 1982 or 1988). After an average follow-up of 21 years, 1,449 persons (73%) aged 65-79 years took part in a reexamination in 1998.RESULTS: Smoking in midlife increased the risk of dementia (odds ratio, OR: 4.93; 95% CI: 1.51-16.11) and AD (OR: 6.56; 95% CI: 1.80-23.94) among the APOE ε4 carriers, but not among the APOE ε4 noncarriers.CONCLUSION: Midlife smoking was associated with an increased risk of dementia and AD later in life only among those individuals carrying the APOE ε4 allele. These results suggest that the association between smoking and AD may be complex and vary according to genotype.
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