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[Mercury and Alzheimer's disease].
Fortschr Neurol Psychiatr. 2007 Sep; 75(9):528-38.FN

Abstract

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.

Authors+Show Affiliations

Institut für Umweltmedizin und Krankenhaushygiene, Universitätsklinik Freiburg (Franz Daschner), Breidacher Strasse 115b, 79106 Freiburg i. Brsg. joachim.mutter@uniklinik-freiburg.deNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

ger

PubMed ID

17628833

Citation

Mutter, J, et al. "[Mercury and Alzheimer's Disease]." Fortschritte Der Neurologie-Psychiatrie, vol. 75, no. 9, 2007, pp. 528-38.
Mutter J, Naumann J, Schneider R, et al. [Mercury and Alzheimer's disease]. Fortschr Neurol Psychiatr. 2007;75(9):528-38.
Mutter, J., Naumann, J., Schneider, R., & Walach, H. (2007). [Mercury and Alzheimer's disease]. Fortschritte Der Neurologie-Psychiatrie, 75(9), 528-38.
Mutter J, et al. [Mercury and Alzheimer's Disease]. Fortschr Neurol Psychiatr. 2007;75(9):528-38. PubMed PMID: 17628833.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Mercury and Alzheimer's disease]. AU - Mutter,J, AU - Naumann,J, AU - Schneider,R, AU - Walach,H, Y1 - 2007/07/12/ PY - 2007/7/14/pubmed PY - 2007/10/30/medline PY - 2007/7/14/entrez SP - 528 EP - 38 JF - Fortschritte der Neurologie-Psychiatrie JO - Fortschr Neurol Psychiatr VL - 75 IS - 9 N2 - 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. SN - 0720-4299 UR - https://www.unboundmedicine.com/medline/citation/17628833/[Mercury_and_Alzheimer's_disease]_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-2007-959237 DB - PRIME DP - Unbound Medicine ER -