Your chances of getting dementia.
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
The useless crap here:
Alzheimer’s Disease Risk Impacted by the Liver, Diet
Reduced
levels of plasmalogens are associated with an increased risk of
Alzheimer’s Disease, according to a study presented at the Alzheimer’s
Association International Conference (AAIC).
Plasmalogens are created in the liver and are dispersed through the bloodstream in the form of lipoproteins.
Mitchel A. Kling, MD, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, and Rima F. Kaddurah-Daouk, PhD, Duke University School of Medicine, Durham, North Carolina, and colleagues developed 3 indices for measuring the amount of these lipids related to cognition, in order to identify whether reduced levels in the bloodstream are associated with an increased risk of Alzheimer’s disease, mild cognitive impairment (MCI), overall cognitive function, and/or other biomarkers of neurodegeneration in Alzheimer’s disease.
The 3 indices measured: the ratios of plasmalogens to each other; the ratios of plasmalogens to their closely-related, more conventional lipid counterparts; and a combination of these 2 quantities.
They measured several plasmalogens including those containing omega-3 fatty acids docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), as well as an omega-6 fatty acid and closely-related non-plasmalogen lipids, in blood-based fluids collected from 2 groups.
The first group included 1,547 subjects with Alzheimer’s disease, MCI or significant memory concerns (SMC), and subjects who were cognitively normal (CN) and who are enrolled in the Alzheimer’s Disease Neuroimaging Initiative. The second group included 112 subjects from the Penn Memory Center, including those with Alzheimer’s, MCI, and CN.
The team observed that lower values of these indices were associated with a higher likelihood of Alzheimer’s disease. A similar pattern was seen with MCI and CN associations. In addition, some of the decreased plasmalogen levels were correlated with increased levels of the tau protein in the brain.
“This research shows that an age-related deficiency of plasmalogens could lead to an increased risk of Alzheimer’s disease, because the liver cannot make enough of them,” said Dr. Kling. “This research has a variety of interesting implications. For example, it highlights a potential relationship between conditions such as obesity and diabetes and Alzheimer’s -- as the liver has to work harder to break down fatty acids over time. This could lead to the eventual destruction of the peroxisomes that create plasmalogens which thus, increases the risk of Alzheimer’s.”
The findings also provide a possible explanation for the observed lack of effect of fish oil or DHA administration on cognitive function or Alzheimer’s disease, which has been shown in other studies. This is due to the defect in the liver that prevents these fatty acids from becoming incorporated into the plasmalogens that are critical for synaptic function in brain, which can affect cognition. Several of the genes associated with Alzheimer’s are involved in lipid transport or metabolism, therefore ongoing research is looking to see how changes in the production or transport of lipids affect brain structure and function.
“Our findings provide renewed hope for the creation of new treatment and prevention approaches for Alzheimer’s disease,” said Dr. Kling. “Moving forward, we’re examining the connections between plasmalogens, other lipids, and cognition, in addition to gene expression in the liver and the brain. While we’re in the early stages of discovering how the liver, lipids, and diet are related to Alzheimer’s disease and neurodegeneration, it’s been promising.”
SOURCE: University of Pennsylvania
Plasmalogens are created in the liver and are dispersed through the bloodstream in the form of lipoproteins.
Mitchel A. Kling, MD, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, and Rima F. Kaddurah-Daouk, PhD, Duke University School of Medicine, Durham, North Carolina, and colleagues developed 3 indices for measuring the amount of these lipids related to cognition, in order to identify whether reduced levels in the bloodstream are associated with an increased risk of Alzheimer’s disease, mild cognitive impairment (MCI), overall cognitive function, and/or other biomarkers of neurodegeneration in Alzheimer’s disease.
The 3 indices measured: the ratios of plasmalogens to each other; the ratios of plasmalogens to their closely-related, more conventional lipid counterparts; and a combination of these 2 quantities.
They measured several plasmalogens including those containing omega-3 fatty acids docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), as well as an omega-6 fatty acid and closely-related non-plasmalogen lipids, in blood-based fluids collected from 2 groups.
The first group included 1,547 subjects with Alzheimer’s disease, MCI or significant memory concerns (SMC), and subjects who were cognitively normal (CN) and who are enrolled in the Alzheimer’s Disease Neuroimaging Initiative. The second group included 112 subjects from the Penn Memory Center, including those with Alzheimer’s, MCI, and CN.
The team observed that lower values of these indices were associated with a higher likelihood of Alzheimer’s disease. A similar pattern was seen with MCI and CN associations. In addition, some of the decreased plasmalogen levels were correlated with increased levels of the tau protein in the brain.
“This research shows that an age-related deficiency of plasmalogens could lead to an increased risk of Alzheimer’s disease, because the liver cannot make enough of them,” said Dr. Kling. “This research has a variety of interesting implications. For example, it highlights a potential relationship between conditions such as obesity and diabetes and Alzheimer’s -- as the liver has to work harder to break down fatty acids over time. This could lead to the eventual destruction of the peroxisomes that create plasmalogens which thus, increases the risk of Alzheimer’s.”
The findings also provide a possible explanation for the observed lack of effect of fish oil or DHA administration on cognitive function or Alzheimer’s disease, which has been shown in other studies. This is due to the defect in the liver that prevents these fatty acids from becoming incorporated into the plasmalogens that are critical for synaptic function in brain, which can affect cognition. Several of the genes associated with Alzheimer’s are involved in lipid transport or metabolism, therefore ongoing research is looking to see how changes in the production or transport of lipids affect brain structure and function.
“Our findings provide renewed hope for the creation of new treatment and prevention approaches for Alzheimer’s disease,” said Dr. Kling. “Moving forward, we’re examining the connections between plasmalogens, other lipids, and cognition, in addition to gene expression in the liver and the brain. While we’re in the early stages of discovering how the liver, lipids, and diet are related to Alzheimer’s disease and neurodegeneration, it’s been promising.”
SOURCE: University of Pennsylvania
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