Mercury and Alzheimer's Disease

jay · Joined: 17 Aug 2007 Posts: 21

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

Archived from group: sci>med>nutrition

drkulacz · Joined: 19 Feb 2008 Posts: 1

On Feb 15, 6:21 pm, jay wrote:
> 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

The data on the age onset of Alzheimer's disease and correlation to
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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