| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
- Komulainen, P, et al.
(författare)
-
Carotid intima-media thickness and cognitive function in elderly women: a population-based study
- 2007
-
Ingår i: Neuroepidemiology. - : S. Karger AG. - 1423-0208 .- 0251-5350. ; 28:4, s. 207-213
-
Tidskriftsartikel (refereegranskat)abstract
- <i>Objective:</i> Several vascular risk factors have been linked to cognitive decline. However, little is known about the association between the atherosclerotic process and cognitive impairment. We investigated whether carotid intima-media thickness (IMT) predicts the risk of cognitive impairment and whether the putative impairment is specific for some cognitive domains. <i>Methods:</i> A 12-year population-based follow-up study was performed for a total of 91 women, aged 60–70 years at baseline. Ultrasonographically assessed carotid artery IMT and the Mini-Mental State Examination test were performed at baseline and 12-year follow-up. A detailed cognitive evaluation for memory and cognitive speed was performed in 2003. The mean of left and right carotid bifurcation IMT was used in the analyses for association with the risk for poor cognitive speed and memory. <i>Results:</i> Increased IMT at baseline was an independent predictor for poor memory (β = –5.004, 95% confidence interval = –7.74 to –2.27; p = 0.001) and cognitive speed (β = 2.562, 95% confidence interval = 1.19–4.94; p = 0.035) at 12-year follow-up after adjustment for age, education, depression, plasma LDL cholesterol, systolic blood pressure, cardiovascular disease, hormone replacement therapy, smoking, alcohol consumption and physical activity. The risk for poor memory (p = 0.023 for linear trend) and cognitive speed (p = 0.070 for linear trend) increased with increasing IMT tertiles. <i>Conclusions:</i> Carotid IMT predicts an increased risk for cognitive impairment, particularly poor memory and cognitive speed, in elderly women.
|
|
| 10. |
- 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.
|
|
| 11. |
|
|
| 12. |
- 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 Ε4 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 Ε4 carriers. Thus, dietary interventions may potentially modify the risk of dementia, particularly among genetically susceptible individuals.
|
|
| 13. |
|
|
| 14. |
- 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.
|
|
| 15. |
|
|
| 16. |
- 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 Ε4 (n = 15) and those who were ApoE Ε4 noncarriers (n = 28), only the right parahippocampal gyrus, with the entorhinal cortex included, reached the level of statistical significance. In cases homozygous for the Ε4 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.
|
|
| 17. |
|
|
| 18. |
|
|
