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• W2099587009 abstract "textabstractThe devastating impact of the loss of cognitive abilities that often accompanies the aging process is feared by many. Despite an increasing number of studies, the precise etiology of the disease is not known yet. There is accumulating evidence that a variety of causes, rather than a single factor, result in impaired cognitive function and the clinical symptoms of dementia. Glucose metabolism, vascular pathology and inflammation have all been suggested to play a role in the development of cognitive impairment and dementia. The main objective of the work described in this thesis was the investigation of potentially modifiable risk factors, including factors involved in glucose metabolism, vascular pathology and inflammation in especially the early stages of the disease process. Furthermore, there have been studies that suggested that in general, possible risk factors that play a role at younger ages may not be important anymore when people survive until higher ages. Therefore, I additionally studied the age-specific effects of these risk factors in several large prospective studies including the Rotterdam Study, the Leiden 85-plus Study, and the PROSPER study, that were complementary with respect to the age of the participants and consequently allowed me to study the association between several potentially modifiable risk factors and cognitive function and decline over a wide age range in the general population. Finally, I investigated suggested preclinical biomarkers of dementia that might be !used to identify people who are at increased risk of developing dementia.I first explored the measurement of cognitive function, with respect to the effect of selection by health and survival on the estimation of cognitive function and decline in epidemiological studies. Chapter 2 showed that selection for health and survival resulted in better age-specific cognitive test scores and less cognitive decline, and that this selection affects both cross-sectional and longitudinal studies. Subsequently, statistical methods handling multiple and missing data did not seem to fully correct for this bias. These results indicated that assessments of cognitive function in the elderly must take particular care in considering possible biases from health selection.In chapter 3, the results from studies on the relation between glucose metabolism and cognitive function were presented. First, I investigated the influence of fasting glucose levels and insulin resistance on cognitive function in non-diabetic elderly from two independent prospective studies: the PROSPER study and the Rotterdam Study (chapter 3.1). Elevated fasting glucose levels and insulin resistance were not associated with worse cognitive function or a higher rate of cognitive decline in elderly subjects without a history of diabetes. These data suggest either a threshold for effects of dysglycaemia on cognitive function, or that factors other than hyperglycaemia-related pathways impair cognition in individuals with frank diabetes. In chapter 3.2, I described the relation between genetically reduced insulin/IGF-1 signaling (IIS) and cognitive function and decline, in participants from the Leiden 85-plus Study, aged 85 years and over. In addition to old age survival, gene!tically reduced IIS seemed to be beneficial for cognitive function in women.Chapter 4 described the relation between vascular and inflammatory factors and cognitive function and decline. In chapter 4.1, I evaluated the age-specificity of the relation between blood pressure and cognitive function by examining the relationship between baseline blood pressure and cognitive function later in life across age groups. The data showed that high blood pressure increased the risk of cognitive impairment up to 75 years, but was associated with better cognitive function thereafter. This could mean that age-specific guidelines for blood pressure management are needed, as the current directive that ’lower is better’ may not apply to blood pressure levels in the very old. In chapter 4.2, I investigated the relation between inflammatory markers and cognitive impairment in the early stages of the development of dementia, and found that systemic markers of inflammation were only moderately associated with cognitive function and decline. Chapter 4.3 described the !relation between serum uric acid, a cardiovascular risk factor as well as a major natural antioxidant, and the risk of dementia and cognitive impairment. The results showed that notwithstanding the associated increased risk of cardiovascular disease, higher levels of uric acid were associated with a decreased risk of dementia and better cognitive function later in life.Chapter 5 showed the investigation of potential preclinical biomarkers of dementia. In chapter 5.1, I described the relation between plasma AI²1-42 and AI²1-40 levels and the risk of dementia and evaluated the influence of time-to-event on this relation. Additionally, I studied the relation between plasma AI²1-42 and AI²1-40 levels and the risk of cognitive decline in those who remained free of dementia. It seemed that the risk of dementia associated with a lower plasma AI²1-42 / AI²1-40 ratio was particularly increased within the first years after the biomarker assessment. There was no association between the plasma AI²1-42 / AI²1-40 ratio and the risk of cognitive decline in those who did not develop dementia. This indicates that assessment of the plasma AI²1-42 / AI²1-40 ratio alone is not sensitive enough to identify people at risk for cognitive decline at large.In chapter 6, I evaluated the several methodological issues that were related to the work described in this thesis and discussed some suggestions for further research." @default.
• W2099587009 created "2016-06-24" @default.
• W2099587009 creator A5059475329 @default.
• W2099587009 date "2008-12-17" @default.
• W2099587009 modified "2023-09-27" @default.
• W2099587009 title "Determinants of Cognitive Decline and Dementia in the Very Old" @default.
• W2099587009 cites W1508589930 @default.
• W2099587009 cites W1556008598 @default.
• W2099587009 cites W1567615384 @default.
• W2099587009 cites W1586213696 @default.
• W2099587009 cites W1618236677 @default.
• W2099587009 cites W1812816875 @default.
• W2099587009 cites W1847168837 @default.
• W2099587009 cites W1859919035 @default.
• W2099587009 cites W1870043354 @default.
• W2099587009 cites W1892420199 @default.
• W2099587009 cites W1894359193 @default.
• W2099587009 cites W1929267935 @default.
• W2099587009 cites W1961179371 @default.
• W2099587009 cites W1965135841 @default.
• W2099587009 cites W1965653222 @default.
• W2099587009 cites W1965801493 @default.
• W2099587009 cites W1967203590 @default.
• W2099587009 cites W1970679043 @default.
• W2099587009 cites W1972120835 @default.
• W2099587009 cites W1973667575 @default.
• W2099587009 cites W1975107311 @default.
• W2099587009 cites W1978209044 @default.
• W2099587009 cites W1978769917 @default.
• W2099587009 cites W1979030376 @default.
• W2099587009 cites W1981148605 @default.
• W2099587009 cites W1982214580 @default.
• W2099587009 cites W1985425785 @default.
• W2099587009 cites W1987444426 @default.
• W2099587009 cites W1992777999 @default.
• W2099587009 cites W1992998861 @default.
• W2099587009 cites W1993383247 @default.
• W2099587009 cites W1995175521 @default.
• W2099587009 cites W1995709472 @default.
• W2099587009 cites W1998664055 @default.
• W2099587009 cites W2003177861 @default.
• W2099587009 cites W2004531476 @default.
• W2099587009 cites W2011575267 @default.
• W2099587009 cites W201521563 @default.
• W2099587009 cites W2016742756 @default.
• W2099587009 cites W2017260345 @default.
• W2099587009 cites W2021391816 @default.
• W2099587009 cites W2021652661 @default.
• W2099587009 cites W2025341690 @default.
• W2099587009 cites W2025514832 @default.
• W2099587009 cites W2025774809 @default.
• W2099587009 cites W2029615800 @default.
• W2099587009 cites W2031187292 @default.
• W2099587009 cites W2031721411 @default.
• W2099587009 cites W2034664059 @default.
• W2099587009 cites W2034916584 @default.
• W2099587009 cites W2034945547 @default.
• W2099587009 cites W2036325014 @default.
• W2099587009 cites W2038686627 @default.
• W2099587009 cites W2039428198 @default.
• W2099587009 cites W2041085272 @default.
• W2099587009 cites W2041851050 @default.
• W2099587009 cites W2042245550 @default.
• W2099587009 cites W2044015546 @default.
• W2099587009 cites W2044976134 @default.
• W2099587009 cites W2045148031 @default.
• W2099587009 cites W2046734715 @default.
• W2099587009 cites W2047683380 @default.
• W2099587009 cites W2049009766 @default.
• W2099587009 cites W2051088635 @default.
• W2099587009 cites W2052990008 @default.
• W2099587009 cites W2056045638 @default.
• W2099587009 cites W2057042201 @default.
• W2099587009 cites W2058614488 @default.
• W2099587009 cites W2060497747 @default.
• W2099587009 cites W2060749333 @default.
• W2099587009 cites W2063098376 @default.
• W2099587009 cites W2065184319 @default.
• W2099587009 cites W2069988949 @default.
• W2099587009 cites W2071051054 @default.
• W2099587009 cites W2071522837 @default.
• W2099587009 cites W2072435649 @default.
• W2099587009 cites W2073481032 @default.
• W2099587009 cites W2077180087 @default.
• W2099587009 cites W2078065085 @default.
• W2099587009 cites W2078103515 @default.
• W2099587009 cites W2078868323 @default.
• W2099587009 cites W2079268021 @default.
• W2099587009 cites W2080129332 @default.
• W2099587009 cites W2082266356 @default.
• W2099587009 cites W2083425457 @default.
• W2099587009 cites W2083644061 @default.
• W2099587009 cites W2084471425 @default.
• W2099587009 cites W2085618125 @default.
• W2099587009 cites W2087255758 @default.
• W2099587009 cites W2087574229 @default.
• W2099587009 cites W2087671869 @default.
• W2099587009 cites W2094418975 @default.
• W2099587009 cites W2096186694 @default.
• W2099587009 cites W2099887180 @default.

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