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| jay wrote: - quote - > 1: Fortschr Neurol Psychiatr. 2007 Sep;
So mayonnaise to the rescue!> [Mercury and Alzheimer's disease] > > Higher mercury concentrations were found in brain regions and blood of > some patients with Alzheimer's disease (AD). Low levels of inorganic > mercury were able to cause AD- typical nerve cell deteriorations in > vitro and in animal experiments. Other metals like zinc, aluminum, > copper, cadmium, manganese, iron, and chrome are not able to elicit > all of these deteriorations in low levels, yet they aggravate the > toxic effects of mercury (Hg). Main human sources for mercury are fish > consumption (Methyl-Hg) and dental amalgam (Hg vapour). Regular fish > consumption reduces the risk of development of AD. Amalgam consists of > approx. 50 % of elementary mercury which is constantly being vaporized > and absorbed by the organism. Mercury levels in brain tissues are 2 - > 10 fold higher in individuals with dental amalgam. Persons showing a > genetically determined subgroup of transportation protein for fats > (apolipoprotein E4) have an increased AD risk. Apoliprotein E (APO E) > is found in high concentrations in the central nervous system. The > increased AD risk through APO E4 might be caused by its reduced > ability to bind heavy metals. Latest therapeutic approaches to the > treatment of Alzheimer disease embrace pharmaceuticals which remove or > bind metals from the brain. Preliminary success has been documented > with chelation of synergistic toxic metals (Fe, Al, Zn, Cu) and > therefore also Hg. The available data does not answer the question, > whether mercury is a relevant risk factor in AD distinctively. In sum, > the findings from epidemiological and demographical studies, the > frequency of amalgam application in industrialized countries, clinical > studies, experimental studies and the dental state of Alzheimer > patients in comparison to controls suggest a decisive role for > inorganic mercury in the etiology of Alzheimer's disease. Other > factors currently discussed as causes (e. g. other metals, > inflammations, dietetic factors, vitamin deficiency, oxidative > distress, and metabolic impairments) may act as co-factors. > > PMID: 17628833 -- Marshall Price of Miami Known to Yahoo as d021317c |
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| On Feb 15, 6:21*pm, jay <jaym1...[at]hotmail.com> wrote: - quote - > 1: Fortschr Neurol Psychiatr. 2007 Sep;
The data on the age onset of Alzheimer's disease and correlation to> [Mercury and Alzheimer's disease] > > Higher mercury concentrations were found in brain regions and blood of > some patients with Alzheimer's disease (AD). Low levels of inorganic > mercury were able to cause AD- typical nerve cell deteriorations in > vitro and in animal experiments. Other metals like zinc, aluminum, > copper, cadmium, manganese, iron, and chrome are not able to elicit > all of these deteriorations in low levels, yet they aggravate the > toxic effects of mercury (Hg). Main human sources for mercury are fish > consumption (Methyl-Hg) and dental amalgam (Hg vapour). Regular fish > consumption reduces the risk of development of AD. Amalgam consists of > approx. 50 % of elementary mercury which is constantly being vaporized > and absorbed by the organism. Mercury levels in brain tissues are 2 - > 10 fold higher in individuals with dental amalgam. Persons showing a > genetically determined subgroup of transportation protein for fats > (apolipoprotein E4) have an increased AD risk. Apoliprotein E (APO E) > is found in high concentrations in the central nervous system. The > increased AD risk through APO E4 might be caused by its reduced > ability to bind heavy metals. Latest therapeutic approaches to the > treatment of Alzheimer disease embrace pharmaceuticals which remove or > bind metals from the brain. Preliminary success has been documented > with chelation of synergistic toxic metals (Fe, Al, Zn, Cu) and > therefore also Hg. The available data does not answer the question, > whether mercury is a relevant risk factor in AD distinctively. In sum, > the findings from epidemiological and demographical studies, the > frequency of amalgam application in industrialized countries, clinical > studies, experimental studies and the dental state of Alzheimer > patients in comparison to controls suggest a decisive role for > inorganic mercury in the etiology of Alzheimer's disease. Other > factors currently discussed as causes (e. g. other metals, > inflammations, dietetic factors, vitamin deficiency, oxidative > distress, and metabolic impairments) may act as co-factors. > > PMID: 17628833 the Apolipoprotein E (APO E) has been known for some time now. APO E4 has no sulfhydryl groups to bind heavy metals. In contrast, APO E2 has two cysteine (each with a heavy metal binding sulfyhdryl group) in place of arginine (with no sulfhydryl group.) APO E3 has one arginine and one cysteine AA.. The remainder of the APO E is the same in APO E2, Apo E3, and APO E4 in its approx 120 amino acid chain. Heavy metals such as mercury have a high affinity for sulfhydryl groups. That is why there is disruption of B-Tubulin in the brain when mercury binds to the sulfhydryul groups disrupting the formation of microtubules. On one extreme, APO E2 may be protective since it has the 2 sulfhydryl cysteine AA, while at the other extreme APO E4 may have no protective effect since it has no heavy metal binding sites. |
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| 1: Fortschr Neurol Psychiatr. 2007 Sep; [Mercury and Alzheimer's disease] Higher mercury concentrations were found in brain regions and blood of some patients with Alzheimer's disease (AD). Low levels of inorganic mercury were able to cause AD- typical nerve cell deteriorations in vitro and in animal experiments. Other metals like zinc, aluminum, copper, cadmium, manganese, iron, and chrome are not able to elicit all of these deteriorations in low levels, yet they aggravate the toxic effects of mercury (Hg). Main human sources for mercury are fish consumption (Methyl-Hg) and dental amalgam (Hg vapour). Regular fish consumption reduces the risk of development of AD. Amalgam consists of approx. 50 % of elementary mercury which is constantly being vaporized and absorbed by the organism. Mercury levels in brain tissues are 2 - 10 fold higher in individuals with dental amalgam. Persons showing a genetically determined subgroup of transportation protein for fats (apolipoprotein E4) have an increased AD risk. Apoliprotein E (APO E) is found in high concentrations in the central nervous system. The increased AD risk through APO E4 might be caused by its reduced ability to bind heavy metals. Latest therapeutic approaches to the treatment of Alzheimer disease embrace pharmaceuticals which remove or bind metals from the brain. Preliminary success has been documented with chelation of synergistic toxic metals (Fe, Al, Zn, Cu) and therefore also Hg. The available data does not answer the question, whether mercury is a relevant risk factor in AD distinctively. In sum, the findings from epidemiological and demographical studies, the frequency of amalgam application in industrialized countries, clinical studies, experimental studies and the dental state of Alzheimer patients in comparison to controls suggest a decisive role for inorganic mercury in the etiology of Alzheimer's disease. Other factors currently discussed as causes (e. g. other metals, inflammations, dietetic factors, vitamin deficiency, oxidative distress, and metabolic impairments) may act as co-factors. PMID: 17628833 |
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| alzheimer, disease, mercury |
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