Date:   8/30/2005 9:45:24 PM ( 19 y ago)
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Title :
Determination of blood mercury concentrations in Alzheimer's patients.
Author :
Fung YK; Meade AG; Rack EP; Blotcky AJ; Claassen JP; Beatty MW; Durham T
Address :
Department of Oral Biology, University of Nebraska Medical Center,
College of Dentistry, Lincoln 68583-0740, USA.
Source :
J Toxicol Clin Toxicol, 1995, 33:3, 243-7

Abstract :
Trace element neurotoxicity can be an etiologic factor for Alzheimer's
disease. This cross sectional clinical study determined blood mercury
in patients with diagnosed Alzheimer's disease as compared to control
subjects without known central nervous system and renal disorders.
Unique within the confines of a nursing home, all subjects were exposed
to the same environment and consumed a diet without fish and seafood
for a period of three months prior to the study. The results of this
study show that blood mercury concentrations detected in subjects with
Alzheimer's disease were not statistically different than that of
control subjects. Ratios of blood mercury to blood selenium were also
determined and no statistical difference was found between these two
groups.
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Title :
Brain mercury in neurodegenerative disorders.
Author :
Fung YK; Meade AG; Rack EP; Blotcky AJ
Address :
Department of Oral Biology, University of Nebraska Medical Center,
College of Dentistry, Lincoln 68583-0740, USA.
Source :
J Toxicol Clin Toxicol, 1997, 35:1, 49-54

Abstract :
BACKGROUND: Trace element neurotoxicity has long been invoked as an
etiologic factor for Alzheimer's disease. This study was conducted to
determine the concentrations of mercury in seven different brain
regions from deceased patients histologically confirmed with
Alzheimer's disease or multiple sclerosis as compared to control
subjects without known central nervous system and renal disorders.
Brain mercury concentrations in all deceased subjects can arise from
amalgam restorations, diet, and the working environment. METHODS:
Autopsy frozen specimens (control, Alzheimer's disease and multiple
sclerosis) from seven brain regions, which included frontal cortex,
temporal cortex, occipital cortex, putamen, hippocampus, corona radiata
and corpus callosum were assayed for the concentrations of selenium
using instrumental neutron activation analysis and mercury using
radiochemical neutron activation analysis. RESULTS: We found that the
concentrations of mercury and the mercury/selenium molar ratios were
significantly lower in the hippocampi of multiple sclerosis patients as
compared to aged-matched controls. However, no statistically
significant differences were detected for the concentrations of mercury
and the mercury/ selenium molar ratios for the remaining six brain
regions among these groups. CONCLUSIONS: Since brain mercury
concentrations from deceased subjects with either Alzheimer's disease
or multiple sclerosis are not significantly higher than controls, the
present study provides no scientific support that mercury plays a
significant role in the pathogenesis of these neurologic disorders.
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Title :
Mercury determination in nursing home patients with Alzheimer's
disease.
Author :
Fung YK; Meade AG; Rack EP; Blotcky AJ; Claassen JP; Beatty MW;
Durham T
Address :
Department of Oral Biology, University of Nebraska Medical Center,
College of Dentistry, Lincoln 68538-0740, USA.
Source :
Gen Dent, 1996 Jan-Feb, 44:1, 74-8

Abstract :
Trace-element neurotoxicity contributing to the development of
Alzheimer's disease (AD) may be an important etiologic factor for this
disorder. This clinical study was conducted to determine the urine
concentrations of mercury (Hg) from patients with AD disorders. Within
the confines of a nursing home, all subjects were exposed to the same
environment and a diet that excluded seafood. The results of this study
do not indicate that subjects with AD have a greater body burden of Hg,
according to urinary excretion. This can be further evidence that Hg
from Amalgam restorations or diet is not related to etiology and
pathogenesis of AD.



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Title :
Mercury and multiple sclerosis.
Author :
Clausen J
Address :
Institute for Life Sciences and Chemistry, Roskilde University,
Denmark.
Source :
Acta Neurol Scand, 1993 Jun, 87:6, 461-4

Abstract :
It has occasionally been claimed that multiple sclerosis (MS) may be
due to a chronic mercury intoxication, e.g. from mercury liberated from
dental fillings. Therefore, the present communication compares the
mercury content assayed by neutron activation in 8 macroscopically
normal areas (frontal lobe) of MS autopsy brains with those of 8
control samples. No significant differences could be traced between the
two groups concerning total mercury. However, the lipid-soluble mercury
(preferably methyl mercury) expressed per cell unit (DNA) was found
significantly decreased in MS. These data may be explained either by a
wash-out of lipid soluble mercury due to break-down of the blood-brain
barrier in MS or to abnormalities in methylation processes probably
related to the vitamin B12 metabolism in MS.






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DMSA and the placebo myth...(PD)

Title :
DMSA administration to patients with alleged mercury poisoning from
dental amalgams: a placebo-controlled study.
Author :
Sandborgh Englund G; Dahlqvist R; Lindelöf B; Söderman E; Jonzon B;
Vesterberg O; Larsson KS
Address :
Department of Odontological Toxicology, Karolinska Institute, Huddinge,
Sweden.
Source :
J Dent Res, 1994 Mar, 73:3, 620-8

Abstract :
The present investigation was performed to determine the effect of
14-day oral administration of meso-2.3-dimercaptosucc inic acid (DMSA)
on the urinary mercury excretion and the potential reduction of blood
and plasma mercury concentrations, and also to relate these effects to
possible decrease of symptoms, allegedly associated with amalgam
fillings. Twenty subjects, relating their symptoms to mercury from
amalgam fillings, received 20 mg/kg DMSA or placebo for 14 days. Their
symptoms and mood states were recorded during the study and at a
check-up 3 months later. Interpretation was based on intra-individual
differences. DMSA-treatment resulted in an average increase in urinary
mercury excretion by 65% and a decrease in blood mercury levels of 0.04
microgram/L/day. At the check-up after 3 months, urinary mercury
excretion had returned to the pre-treatment level. No treatment effect
of DMSA was apparent on subjective symptoms and mood state. One
statistically significant treatment effect was noted-a decrease in
fatigue-inertia in the DMSA-group-but there was no demonstrable
correlation with increased urinary excretion or decreased blood
concentration of mercury. Three subjects showed hypersensitive
reactions, probably DMSA-specific, at the end of the treatment period.
This placebo-controlled study provides no scientific support for
diagnostic or therapeutic administration of DMSA for symptoms allegedly
associated with chronic mercury exposition from dental amalgam
fillings.


 

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