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Sökning: L773:1420 8008 > Soininen H

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1.
  • 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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2.
  • 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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3.
  • Liu, YW, et al. (författare)
  • APOE ε2 allele is associated with larger regional cortical thicknesses and volumes
  • 2010
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 30:3, s. 229-237
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background:</i> The protective effect of the apolipoprotein E (APOE) &#917;2 allele against Alzheimer’s disease (AD) is controversial. <i>Objective:</i> Our purpose was to clarify if the &#917;2 allele affects regional cortical thicknesses and volumes. <i>Methods:</i> Regional cortical thicknesses and volumes were measured with an automated pipeline in 109 subjects with mild cognitive impairment, 114 AD patients and 105 age-matched healthy controls. <i>Results:</i> In the mild cognitive impairment group, the &#917;2 carriers had thicker regional cortices at the transverse temporal cortex and parahippocampal gyrus than the subjects with &#917;3/&#917;3, and a larger cerebral gray matter and smaller lateral ventricles than the &#917;3/&#917;3 and &#917;4 carriers. In the AD group, the &#917;2 carriers had significantly thicker entorhinal and transverse temporal cortices, a larger whole cerebral gray matter, and smaller lateral ventricles than the subjects with the &#917;3/&#917;3 genotype, and a significantly thicker entorhinal cortex and larger cerebral gray matter than &#917;4 carriers. No APOE2 effect was found in the control group. <i>Conclusion:</i> The APOE &#917;2 allele is associated with larger regional cortical thicknesses and volumes in mild cognitive impairment and AD.
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4.
  • 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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5.
  • Norberg, Joakim, et al. (författare)
  • Regional Differences in Effects of APOE epsilon 4 on Cognitive Impairment in Non-Demented Subjects
  • 2011
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 32:2, s. 135-142
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The APOE epsilon 4 allele is a risk factor for Alzheimer's disease (AD). APOE epsilon 4 is common in non-demented subjects with cognitive impairment. In both healthy people and people with AD, its prevalence has a north-south gradient across Europe. In the present study, we investigated whether the relation between the APOE epsilon 4 allele and cognitive impairment varied across Northern, Middle and Southern Europe. We also investigated whether a north-south gradient existed in subjects with subjective cognitive impairment (SCI), amnestic mild cognitive impairment (MCI) and non-amnestic MCI. Methods: Data from 16 centers across Europe were analyzed. Results: A north-south gradient in APOE epsilon 4 prevalence existed in the total sample (62.7% for APOE epsilon 4 carriers in the northern region, 42.1% in the middle region, and 31.5% in the southern region) and in subjects with SCI and amnestic MCI separately. Only in Middle Europe was the APOE epsilon 4 allele significantly associated with poor performance on tests of delayed recall and learning, as well as with the amnestic subtype of MCI. Conclusion: The APOE epsilon 4 allele frequencies in subjects with SCI and amnestic MCI have a north-south gradient. The relation between the APOE epsilon 4 allele and cognition is region dependent.
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6.
  • Norberg, J, et al. (författare)
  • Regional differences in effects of APOE ε4 on cognitive impairment in non-demented subjects
  • 2011
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1421-9824 .- 1420-8008. ; 32:2, s. 135-142
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background:</i> The <i>APOE</i> ε4 allele is a risk factor for Alzheimer’s disease (AD). <i>APOE</i> ε4 is common in non-demented subjects with cognitive impairment. In both healthy people and people with AD, its prevalence has a north-south gradient across Europe. In the present study, we investigated whether the relation between the <i>APOE</i> ε4 allele and cognitive impairment varied across Northern, Middle and Southern Europe. We also investigated whether a north-south gradient existed in subjects with subjective cognitive impairment (SCI), amnestic mild cognitive impairment (MCI) and non-amnestic MCI. <i>Methods:</i> Data from 16 centers across Europe were analyzed. <i>Results:</i> A north-south gradient in <i>APOE</i> ε4 prevalence existed in the total sample (62.7% for <i>APOE</i> ε4 carriers in the northern region, 42.1% in the middle region, and 31.5% in the southern region) and in subjects with SCI and amnestic MCI separately. Only in Middle Europe was the <i>APOE</i> ε4 allele significantly associated with poor performance on tests of delayed recall and learning, as well as with the amnestic subtype of MCI. <i>Conclusion:</i> The <i>APOE</i> ε4 allele frequencies in subjects with SCI and amnestic MCI have a north-south gradient. The relation between the <i>APOE</i> ε4 allele and cognition is region dependent.
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7.
  • 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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8.
  • 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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9.
  • Tervo, S, et al. (författare)
  • Incidence and risk factors for mild cognitive impairment: a population-based three-year follow-up study of cognitively healthy elderly subjects
  • 2004
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 17:3, s. 196-203
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background: </i>Mild cognitive impairment (MCI) has attracted considerable interest as a potential predictor of Alzheimer’s disease (AD). Both the apolipoprotein E (ApoE) &#917;4 allele and vascular factors have been associated with a higher risk for AD, recently they have also been linked to the risk of MCI. <i>Objectives: </i>To estimate the incidence of MCI among cognitively healthy elderly subjects during a 3-year follow-up, and to evaluate the impact of demographic and vascular factors as well as the ApoE &#917;4 allele on the conversion to MCI. <i>Methods: </i>At baseline, the cognitive abilities of 806 out of 1,150 eligible subjects (aged 60–76 years) from a population-based sample were examined. Cognitively intact subjects (n = 747) were followed for an average of 3 years. <i>Results: </i>66 subjects (8.8%) had converted to MCI. The global incidence rate of MCI was 25.94/1,000 person-years. Persons with higher age (OR 1.08, 95% CI 1.01–1.16), ApoE &#917;4 allele carriers (OR 2.04, 95% CI 1.15–3.64) and persons with medicated hypertension (OR 1.86, 95% CI 1.05–3.29) were more likely to convert to MCI than those individuals of lower age and without an ApoE &#917;4 allele or medicated hypertension. Persons with high education (OR 0.79, 95% CI 0.70–0.89) were less likely to convert to MCI than persons with low or no education. In subjects with both the ApoE &#917;4 allele and medicated hypertension, the crude OR for conversion was 3.92 (95% CI 1.81–8.49). In subjects with cardiovascular disease, the crude OR for conversion was 2.13 (95% CI 1.26–3.60). Gender, elevated blood pressure, diabetes or cerebrovascular disease had no significant effect on the conversion to MCI. <i>Conclusion:</i> Higher age, the presence of at least one ApoE &#917;4 allele and medicated hypertension are independent risk factors, but high education is a protective factor for MCI. The results suggest that vascular factors may have an important role in the pathogenesis of MCI.
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10.
  • Wimo, A, et al. (författare)
  • An economic evaluation of donepezil in mild to moderate Alzheimer's disease: results of a 1-year, double-blind, randomized trial
  • 2003
  • Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 15:1, s. 44-54
  • Tidskriftsartikel (refereegranskat)abstract
    • The costs and consequences of donepezil versus placebo treatment in patients with mild to moderate Alzheimer’s disease (AD) were evaluated as part of a 1-year prospective, double-blind, randomized, multinational clinical trial. Patients received either donepezil (n = 142; 5 mg/day for 28 days followed by 10 mg/day according to the clinician’s judgement) or placebo (n = 144). Unit costs were assessed in 1999 Swedish kronas (SEK) and converted to US dollars (USD). Donepezil-treated patients gained functional benefits relative to placebo on the Progressive Deterioration Scale (p = 0.042) and Instrumental Activities of Daily Living scale (p = 0.025) at week 52. Caregivers of donepezil-treated patients spent an average of 400 h less annually providing care than caregivers of placebo-treated patients. Mean annual healthcare costs were SEK 137,752 (USD 16,438) per patient for the donepezil group and SEK 135,314 (USD 16,147) in the placebo group. With the average annual cost of donepezil at SEK 10,723 (USD 1,280) per patient, the SEK 2,438 (USD 291) cost difference represented a 77% cost offset. When caregiver time and healthcare costs were included, mean annual costs were SEK 209,244 (USD 24,969) per patient in the donepezil group and SEK 218,434 (USD 26,066) in the placebo group, a total saving associated with donepezil treatment of SEK 9,190 (USD 1,097) per patient [95% CI of SEK –43,959 (USD –5,246), SEK 25,581 (USD 3,053); p = 0.6]. The positive effects on the efficacy outcome measures combined with no additional costs from a societal perspective indicate that donepezil is a cost-effective treatment, representing an improved strategy for the management of patients with AD.
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