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- Komulainen, P, et al.
(författare)
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Carotid intima-media thickness and cognitive function in elderly women: a population-based study
- 2007
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Ingår i: Neuroepidemiology. - : S. Karger AG. - 1423-0208 .- 0251-5350. ; 28:4, s. 207-213
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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.
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- Komulainen, P, et al.
(författare)
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Metabolic syndrome and cognitive function: a population-based follow-up study in elderly women
- 2007
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Ingår i: Dementia and geriatric cognitive disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 23:1, s. 29-34
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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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- Karpanen, Terhi, et al.
(författare)
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Overexpression of vascular endothelial growth factor-B in mouse heart alters cardiac lipid metabolism and induces myocardial hypertrophy
- 2008
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Ingår i: Circulation Research. - : American Heart Association. - 0009-7330 .- 1524-4571. ; 103:9, s. 1018-1026
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Tidskriftsartikel (refereegranskat)abstract
- Vascular endothelial growth factor (VEGF)-B is poorly angiogenic but prominently expressed in metabolically highly active tissues, including the heart. We produced mice expressing a cardiac-specific VEGF-B transgene via the alpha-myosin heavy chain promoter. Surprisingly, the hearts of the VEGF-B transgenic mice showed concentric cardiac hypertrophy without significant changes in heart function. The cardiac hypertrophy was attributable to an increased size of the cardiomyocytes. Blood capillary size was increased, whereas the number of blood vessels per cell nucleus remained unchanged. Despite the cardiac hypertrophy, the transgenic mice had lower heart rate and blood pressure than their littermates, and they responded similarly to angiotensin II-induced hypertension, confirming that the hypertrophy does not compromise heart function. Interestingly, the isolated transgenic hearts had less cardiomyocyte damage after ischemia. Significantly increased ceramide and decreased triglyceride levels were found in the transgenic hearts. This was associated with structural changes and eventual lysis of mitochondria, resulting in accumulation of intracellular vacuoles in cardiomyocytes and increased death of the transgenic mice, apparently because of mitochondrial lipotoxicity in the heart. These results suggest that VEGF-B regulates lipid metabolism, an unexpected function for an angiogenic growth factor.
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