Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case-control study was conducted among the multiethnic population of Singapore to test the hypothesis that a high level of body burden mercury is associated with an increased risk of Parkinson's disease (PD). Selected factors investigated that could contribute to the body burden of mercury included dietary fish intake, ethnic over-the-counter medications, occupational exposures and possession of dental amalgam fillings. Detailed interviews were completed in 54 cases of idiopathic PD and 95 hospital-based controls, matched for age, sex and ethnicity, between July 1985 and July 1987. After adjusting for potential confounding factors, including dietary fish intake, medications, smoking and alcohol consumption, there was clear monotonic dose-response association between PD and blood mercury levels. The odds ratios (OR) and 95% confidence intervals (CI) for the approximate subject tertiles based upon blood mercury levels were 8.5 (CI = 2.2-33.2) and 9.4 (CI = 2.5-35.9), relative to the tertile with lowest blood mercury levels (less than 5.8 ng Hg/ml). Similar associations were revealed using scalp hair and urinary mercury levels. However, only the comparisons between the highest and lowest tertiles were statistically different from unity (p less than 0.05). When the body burden mercury indicators were mutually adjusted in addition to the four confounding factors, blood and urinary mercury levels showed ORs of 21.00 and 18.65, respectively. These ORs were statistically different from unity (p less than 0.05, 2-sided test). After adjustment, scalp hair mercury was shown to be a poor predictor of PD risk.
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PMID:Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson's disease. 272 5

In middle of Kii peninsula, one of the biggest mercury mine in Japan had been present until about 10 years ago. The mercury contents in water and fish are reported to be higher in this district. So we investigated the mercury in hair of patients and normal controls. In this study the subjects are 23 cases of ALS including 15 cases in Nara and Mie and 8 cases in other prefectures except in Kii peninsula, 14 cases with ataxia, 11 cases with other degenerative diseases like Parkinson's disease and Alzheimer's disease, 25 cases of cerebrovascular disease as compared to 26 normal controls. The hair are taken from 3 areas on head of patients and normal controls. They are washed in 2% sodium lauryl sulfate and stirred in distilled water several times, and they are soaked in acetone and dried in filter paper. They are inserted in fire and vaporized mercury are measured (Zeeman Effect Mercury Analyzer) in ppm. The hair mercury concentration is 2.81 ppm in ALS in total, 3.62 ppm in ALS in Nara and Mie and 1.39 ppm in outside of Kii Peninsula, 2.34 ppm in ataxia, 1.83 ppm in other degenerative diseases, 1.66 ppm in cerebrovascular disease and 1.44 ppm in normal controls. Statistically it is significant (p less than 0.05) between that in ALS in Nara and Mie and that in normal controls. 6 cases (40%) with ALS in Nara and Mie have the value above the mean +2 standard deviation of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mercury in hair of patients with ALS]. 280 5

Parkinson's disease has been associated with heavy occupational exposure to carbon disulfide, and this solvent, as well as other organic solvents, may cause neurotoxic effects. Therefore, the hypothesis was raised that organic solvents in general may be associated with Parkinson's disease. A case-referent study design was applied, and some other suspected exposures were studied as well. The diagnosis registers of two Swedish hospitals were used as the source of subjects. Male in-patients with Parkinson's disease (the cases) or subarachnoid hemorrhage (referents), with symptom appearance between 35-69 a of age and residence in the vicinity of the hospitals, were included in the study. Occupational exposure to the chemicals under study were determined from questionnaire answers of 91 cases and 75 referents. No differences in exposure frequency to organic solvents in general were observed, but three cases had been exposed to carbon disulfide compared to none of the referents. Six cases, but only two referents, had been exposed to mercury, and further exploration of a possible association between exposure to mercury and Parkinson's disease is recommended. The outcome of the study does not support the hypothesis that occupational exposure to organic solvents in general increases the risk of Parkinson's disease, but the confidence intervals of the odds ratios do not rule out such possibilities.
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PMID:Parkinson's disease and occupational exposure to organic solvents, agricultural chemicals and mercury--a case-referent study. 734 10

We studied the relative etiologic importance upon the development of Parkinson's disease (PD) of occupational exposure to herbicides and other compounds, ionizing radiation exposure, family history of PD and essential tremor, smoking, and history of various viral and other medical conditions. We identified patients (n = 130) with neurologist-confirmed idiopathic PD through contacts with Calgary general hospitals, long-term care facilities, neurologists, the Movement Disorder Clinic, and the Parkinson's Society of Southern Alberta, and selected two matched (by sex and age +/- 2.5 years) community controls for each case by random digit dialing. We obtained lifetime work, chemical, radiation, medical, and smoking exposure histories and family histories of PD and essential tremor by personal interviews, and analyzed the data using conditional logistic regression for matched sets. After controlling for potential confounding and interaction between the exposure variables, using multivariate statistical methods, having a family history of PD was the strongest predictor of PD risk, followed by head trauma and then occupational herbicide use. Cases and controls did not differ in their previous exposures to smoking or ionizing radiation; family history of essential tremor; work-related contact with aluminum, carbon monoxide, cyanide, manganese, mercury, or mineral oils; or history of arteriosclerosis, chicken pox, encephalitis, hypertension, hypotension, measles, mumps, rubella, or Spanish flu. These results support the hypothesis of a multifactorial etiology for PD, probably involving genetic, environmental, trauma, and possibly other factors.
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PMID:Parkinson's disease: a test of the multifactorial etiologic hypothesis. 817 May 64

Parkinson's disease (PD) mortality rates in Michigan counties for 1986-1988 were calculated with respect to potential heavy metal exposure (iron, zinc, copper, mercury, magnesium, and manganese) from industry based on recent census data. Individuals were counted as a PD death if the diagnosis was listed as an "underlying" or "related" cause of death on the death certificate. Counties with an industry in the paper, chemical, iron, or copper related-industrial categories (ICs) had statistically significantly (p < 0.05) higher PD death rates than counties without these industries. Significant correlations of chemical (rs = 0.22; p = 0.05), paper (rs = 0.22; p = 0.05) and iron (rs = 0.29; p = 0.008) industry densities with PD death rates were also present. Counties were divided into high (> 15/100,000 individuals 45 years old and over) and low (< = 15/100,000) PD death rate counties by cluster analysis. Geographically, counties with high PD mortality were located mainly in the southern half of the lower peninsula and eastern half of the upper peninsula; low PD death rate counties formed two distinct clusters in the western edge of the upper peninsula and the north-central portion of the lower peninsula. Other possible risk factors that may explain the varied distribution of PD death rates in Michigan were examined. Those significantly correlated with PD mortality included population density (rs = 0.31; p = 0.005), farming density (rs = 0.25; p = 0.02), and well water use (rs = -0.24; p = 0.03). These ecologic findings suggest a geographic association between PD mortality and the industrial use of heavy metals.
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PMID:Parkinson's disease mortality and the industrial use of heavy metals in Michigan. 841 12

In a population-based case-control study, we investigated the potential role of occupational exposure to iron, copper, manganese, mercury, zinc, and lead as risk factors for Parkinson's disease (PD). Concurrently recruited, nondemented patients (n = 144) with idiopathic PD and controls (n = 464) consisting of men and women > or =50 years of age, frequency-matched for age (within 5 years), race, and sex were enrolled. All had primary medical care at Henry Ford Health System in urban/suburban metropolitan Detroit. Subjects were given an extensive risk-factor questionnaire detailing actual worksite conditions of all jobs held for more than 6 months from age 18 onward. An industrial hygienist, blinded to the case-control status of subjects, rated occupational exposure to each of the metals of interest. When adjusted for sex, race, age, and smoking status, we found in those with more than 20 years' exposure a significantly increased association with PD for copper (OR = 2.49, 95% CI = 1.06, 5.89) and manganese (OR = 10.61, 95% CI = 1.06, 105.83). For more than 20 years' exposure to combinations of lead-copper (OR = 5.24, 95% CI = 1.59, 17.21), lead-iron (OR = 2.83, 95% CI = 1.07, 7.50), and iron-copper (OR = 3.69, 95% CI = 1.40, 9.71), there was a greater association with PD than with any of these metals alone. These findings suggest that chronic exposure to these metals is associated with PD, and that they may act alone or together over time to help produce the disease.
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PMID:Occupational exposures to metals as risk factors for Parkinson's disease. 906 42

Depletion of reduced glutathione occurs in the substantia nigra in Parkinson's disease and in incidental Lewy body disease (presymptomatic Parkinson's disease) which may implicate oxidative stress in the neurodegenerative process. In this study mercury orange fluorescent staining and immunostaining with an antibody to reduced glutathione have been used to determine the distribution of reduced glutathione in the substantia nigra in Parkinson's disease compared with normal individuals. Mercury orange staining showed moderate background levels of fluorescence in the neuropil in both control and Parkinson's disease substantia nigra and localised reduced glutathione to the somata of melanized nigral neurons and glial elements of the neuropil. Neuronal nuclei revealed a relative lack of fluorescence after mercury orange staining. There was a significant depletion of reduced glutathione in surviving neurons in Parkinson's disease compared to nerve cell populations in control tissue. Mercury orange fluorescence indicated a high concentration of reduced glutathione in a subpopulation of non-neuronal cells, most likely astrocytes or microglia. Immunohistochemical examination of nigral tissue from the same Parkinson's disease and control patients with an antibody to glutathione showed staining in neuronal perikarya and axonodendritic processes of melanized nigral neurons which was generally most intense in control neurons. Moderately intense staining of the background neuropil, most prominent in control nigras, and staining of capillary walls was also detected. Intense staining was seen in cells with the morphological features of glial cells in both control and PD nigra. These data show a significant presence of reduced glutathione in the cell bodies and axons of nigral neurons. They are in agreement with biochemical studies showing depletion of reduced glutathione in substantia nigra in Parkinson's disease, and indicate a significant loss of neuronal reduced glutathione in surviving nigral neurons in Parkinson's disease.
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PMID:Alterations in the distribution of glutathione in the substantia nigra in Parkinson's disease. 944 66

Hot, humid conditions in tropical regions generally rule out any risk of hypothermia due to cold exposure. In this report, we describe a case of severe hypothermia involving a core temperature of 26 degrees C in a 61-year-old man living in Gabon. Parkinson's disease and chronic alcoholism may have been predisposing factors. The patient was treated by active and passive rewarming (intestinal irrigation with warm water). Sudden circulatory collapse occurred during treatment but the final outcome was successful. This case demonstrates that hypothermia can occur in tropical areas. Emergency diagnosis may be difficult in Black Africa where adequate temperature monitoring equipment is rarely available. Standard mercury thermometers do not allow measurement of temperatures lower than 34 degrees C. African physicians should be aware of the possibility of potentially life-threatening hypothermia and be prepared to initiate proper treatment and surveillance in intensive care.
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PMID:[Severe hypothermia in a tropical setting]. 979 96

To quantify rapid and precise proximo-distal movements, we have developed a simple system (eurythmokinesimeter or EKM) which requires the subject to touch alternately the center of proximal and distal targets with a stylus. Ninety-six participants, including 30 controls subjects, 36 Cree subjects exposed to mercury, 21 subjects with Parkinson disease, 6 with presumed cerebellar deficit, and 3 with essential tremor, participated in the study. A total of nine measures, including precision, imprecision, contact duration, unsureness, tremor, transit time, irregularity, speed, and Fitts' constant, were calculated. Test-retest reliability was above 0.8 for most measures and above 0.9 for many measures. Correlations between measures and number of outliers with respect to the control group distribution for each measure were used to reduce the set of measures to five (i.e., precision, imprecision, tremor, Fitts' constant, and irregularity). An ANOVA on the three largest groups generated significant results for tremor, Fitts' constant, and irregularity between the Cree and the control subjects and on Fitts' constant and irregularity between the subjects with Parkinson's disease and the control subjects. Three subgroups of the same mean age composed of six subjects each were selected. One was composed of Cree subjects with the highest level of mercury exposure, another with Cree subjects having a low level of mercury exposure, and a third with control subjects. An ANOVA on these three groups revealed a significant difference between both groups of Cree subjects and the control group for Fitts' constant and irregularity. These preliminary results suggest that the EKM system is able to discriminate the performance of different groups of subjects.
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PMID:Quantitative analysis of rapid pointing movements in Cree subjects exposed to mercury and in subjects with neurological deficits. 993 Dec 27

A population-based case-control study was conducted in the Henry Ford Health System (HFHS) in metropolitan Detroit to assess occupational exposures to manganese, copper, lead, iron, mercury and zinc as risk factors for Parkinson's disease (PD). Non-demented men and women 50 years of age who were receiving primary medical care at HFHS were recruited, and concurrently enrolled cases (n = 144) and controls (n = 464) were frequency-matched for sex, race and age (+/- 5 years). A risk factor questionnaire, administered by trained interviewers, inquired about every job held by each subject for 6 months from age 18 onward, including a detailed assessment of actual job tasks, tools and environment. An experienced industrial hygienist, blinded to subjects' case-control status, used these data to rate every job as exposed or not exposed to one or more of the metals of interest. Adjusting for sex, race, age and smoking status, 20 years of occupational exposure to any metal was not associated with PD. However, more than 20 years exposure to manganese (Odds Ratio [OR] = 10.61, 95% Confidence Interval [CI] = 1.06, 105.83) or copper (OR = 2.49, 95% CI = 1.06,5.89) was associated with PD. Occupational exposure for > 20 years to combinations of lead-copper (OR = 5.24, 95% CI = 1.59, 17.21), lead-iron (OR = 2.83, 95% CI = 1.07,7.50), and iron-copper (OR = 3.69, 95% CI = 1.40,9.71) was also associated with the disease. No association of occupational exposure to iron, mercury or zinc with PD was found. A lack of statistical power precluded analyses of metal combinations for those with a low prevalence of exposure (i.e., manganese, mercury and zinc). Our findings suggest that chronic occupational exposure to manganese or copper, individually, or to dual combinations of lead, iron and copper, is associated with PD.
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PMID:Occupational exposure to manganese, copper, lead, iron, mercury and zinc and the risk of Parkinson's disease. 1038 87


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