Brain mercury in neurodegenerative disorders.

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.

Mercury determination in nursing home patients with Alzheimer's disease.

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.

Determination of blood mercury concentrations in Alzheimer's patients.

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.

Determination of aluminum by chemical and instrumental neutron activation analysis in biological standard reference material and human brain tissue.

Since aluminum is an extremely difficult element to determine reliably in biological samples, no National Institute of Standards and Technology (NIST) biological standard reference material for tissue has yet been certified for aluminum. A chemical neutron activation analysis procedure employing anion-exchange chromatography was developed. The procedure proved successful in decontaminating radioactivatable sodium and chlorine and phosphorus which can produce aluminum via a fast neutron bombardment. For bovine liver (NIST SRM 1577 a) a value of 2.1 +/- 0.2 micrograms of aluminum/g of sample was determined, comparing favorably to the uncertified value 2 micrograms/g sample. For freeze-dried urine (NIST SRM 2670) a value of 0.18 +/- 0.01 micrograms of aluminum/mL of urine was observed. Its uncertified value is 0.18 micrograms of aluminum/mL of sample. Twenty three individual samples in three different human brains were analyzed for their aluminum content.

Evidence of aluminum absorption from the gastrointestinal tract and bone deposition by aluminum carbonate ingestion with normal renal function.

The question of whether aluminum is toxic in patients ingesting large oral loads, either for phosphate binding in renal dialysis or as an antacid for peptic ulcer, has been raised. The permeability of the gut barrier for aluminum has not been established because of the lack of precise analytical techniques. Urine aluminum was measured in this study before and during oral aluminum carbonate loading in six subjects with normal renal function, one of which had peptic ulcer disease and a 25-year history of high oral aluminum ingestion. The analytical procedure involved destructive neutron activation analysis. Aluminum was present in the urine in all instances before loading and rose in every case from 4-fold to 10-fold. Bone aluminum was measured in six autopsy specimens, three dialysis patients, three nondialysis patients, and in an iliac crest biopsy from the peptic ulcer patient who had osteoporosis. The bone biopsy aluminum level in the ulcer patient was intermediate between those of "normal subjects" and patients on dialysis. These results show that the gut barrier is permeable to heavy aluminum load and suggest that bone aluminum deposition occurs in humans with normal renal function.