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Fortschr Neurol Psychiatr 2007; 75(9): 528-538
DOI: 10.1055/s-2007-959237
Übersicht
© Georg Thieme Verlag Stuttgart · New York

Quecksilber und Alzheimer-Erkrankung

Mercury and Alzheimer’s DiseaseJ.  Mutter1 , J.  Naumann1 , R.  Schneider1, 2 , H.  Walach1, 2, 3
  • 1Institut für Umweltmedizin und Krankenhaushygiene, Universitätsklinik Freiburg (Franz Daschner)
  • 2Samueli Institute, European Office, Northampton
  • 3School for Social Sciences, University of Northampton, UK
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Publication History

Publication Date:
12 July 2007 (online)

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Zusammenfassung

Bei Personen, welche von der Alzheimer-Demenz (AD) betroffen waren, fanden sich z. T. erhöhte Quecksilberkonzentrationen in Gehirnproben und Blut. Experimentell konnte in Tierexperimenten und in vitro gezeigt werden, dass schon geringste Mengen von Quecksilber in der Lage sind, AD-typische Nervenzellveränderungen auszulösen. Andere Metalle wie Zink, Aluminium, Kupfer, Blei, Cadmium, Mangan, Eisen, Chrom konnten dabei in niedrigen Konzentrationen diese Veränderungen nicht verursachen, steigerten aber die toxischen Wirkungen von Quecksilber (Hg).

Die Hauptquellen der menschlichen Quecksilberbelastung sind Fisch (Methyl-Hg) und Amalgam (Hg-Dampf). Regelmäßiger Fischkonsum scheint das Risiko, an der Alzheimer-Demenz zu erkranken, zu reduzieren. Amalgam besteht aus etwa 50 % Quecksilber, welches aus den Füllungen kontinuierlich freigesetzt und z. T. vom Organismus aufgenommen wird. Amalgamfüllungen führen dabei zu 2 - 10-fach höheren Quecksilberkonzentrationen im Gehirngewebe.

Personen, welche erblich bedingt eine bestimmte Untergruppe eines Transportproteins für Fette aufweisen (Apolipoprotein E4), haben ein erhöhtes AD-Risiko. Dies könnte dadurch bedingt sein, dass APO E4 Schwermetalle nicht gut binden kann. Neuere Therapieansätze zur Behandlung der Alzheimer-Erkrankung beinhalten u. a. die Gabe von Medikamenten, welche Metalle aus dem Gehirn entfernen. Erste Erfolge wurden mit der Gabe von Chelatbildnern, welche synergistisch toxisch wirkende Metalle (Fe, Al, Zn, Cu) und auch Hg entfernen oder binden können, erzielt. Aufgrund der zurzeit bestehenden Datenlage lässt sich die Frage, ob Hg ein maßgeblicher pathogener Faktor für AD ist, nicht eindeutig beantworten. Die zusammenfassende Berücksichtigung der Erkenntnisse aus epidemiologischen und demografischen Studien und der wichtigsten Quecksilberexpositionsquellen in Industrieländern sowie klinischen und experimentellen Studien und schließlich dem Zahnzustand von Alzheimer-Patienten im Vergleich zu Kontrollen lassen eine Rolle von Quecksilber bei der Entstehung der Alzheimererkrankung als möglich erscheinen. Andere Faktoren, welche als (Teil)Ursachen diskutiert werden (z. B. andere Metalle, chronische Entzündungsprozesse, Ernährungsfaktoren, Vitaminmangel, oxidativer Stress, metabolische Beeinträchtigungen usw.), könnten dabei als Kofaktoren angesehen werden.

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.

Schlüsselwörter

Alzheimer - Demenz - Quecksilber - Amalgam - Metalle - Neurotoxizität

Key words

Alzheimer' disease - dementia - mercury - dental amalgam - metals - neurotoxicity

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Dr. Joachim Mutter

Universitätsklinik Freiburg, Institut für Umweltmedizin und Krankenhaushygiene

Breisacher Str. 115b

79106 Freiburg i. Brsg.

Email: joachim.mutter@uniklinik-freiburg.de

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