TY - JOUR
T1 - Brain mercury in neurodegenerative disorders
AU - Fung, Yiu K.
AU - Meade, Andrew G.
AU - Rack, Edward P.
AU - Blotcky, Alan J.
N1 - Funding Information:
We would like to thank John Claassen, James Rhiel, Lisa A. Kanaley-Andrews, and Stephanie L e d for their assistance. Brain tissues from the National Neurological Research Tissue Bank, VAMC, Los Angeles, CA, sponsored by "DS/NIMH, National Multiple Sclerosis Society, Hereditary Disease Foundation, Comprehensive Epilepsy Program, Tourette Syndrome Association, Dystonia Medical Research Foundation, and Department of Veteran Affairs. Brain tissues from McLean Hospital, Belmont, MA, supported in part by PHS grant #MWNS 31862. This research was supported by funding from Wallace Genetic Foundation, Inc., New York and further supported by Veterans Administration Research Funds. This manuscript is written in memory of Dr. Rack for his contribution to research in radioanalytical chemistry.
PY - 1997
Y1 - 1997
N2 - 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.
AB - 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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U2 - 10.3109/15563659709001165
DO - 10.3109/15563659709001165
M3 - Article
C2 - 9022652
AN - SCOPUS:0031042131
SN - 0731-3810
VL - 35
SP - 49
EP - 54
JO - Journal of Toxicology - Clinical Toxicology
JF - Journal of Toxicology - Clinical Toxicology
IS - 1
ER -