A pilot study of risk factors for dementia in Parkinson's disease

To determine whether the risk factors for dementia in idiopathic Parkinson's disease (IPD) are similar to the risk factors for Alzheimer's disease, we conducted a case-control study of potential risk factors. A structured interview was administered to surrogates of 17 demented subjects with IPD and 54 nondemented subjects. Two factors emerged as possible risks for dementia. Demented patients were older than nondemented patients, although the duration of symptoms was similar. A family history of dementia was present in 30% of the demented group and 5.6% of the nondemented group. Dementia was most often reported among siblings. No difference was seen in toxic and occupational exposure, personal habits, or medical or surgical illnesses. We conclude that dementia in IPD shares some common risk factors with Alzheimer's disease. Efforts to assess the contribution of genetic susceptibility or shared environmental influences may clarify the relationship between these two diseases.     

Occupational and environmental risk factors for Parkinson's disease

The etiology of Parkinson's disease (PD) remains obscure. Current research suggests that a variety of occupational and environmental risk factors may be linked to PD. This paper provides an overview of major occupational and environmental factors that have been associated with the development of PD and tries to assess current thinking about these factors and their possible mechanisms of operation. While clear links to rural living, dietary factors, exposure to metals, head injury, and exposure to infectious diseases during childhood have not been established, there is general agreement that smoking and exposure to pesticides affect the probability of developing PD.     

A case-control study of twin pairs discordant for Parkinson's disease: a search for environmental risk factors

A previous study of twins with Parkinson's disease (PD) revealed low concordance, suggesting that genetic factors play a minor role in the etiology of PD. To identify possible environmental determinants of PD while maximally controlling for hereditary factors, 31 monozygotic twin pairs discordant for PD were interviewed by telephone. Information about possible risk factors was obtained from systematic and uniform interviews with cases and controls. The only statistically significant result was less cigarette smoking by PD patients (p less than 0.05). Thirteen dizygotic discordant twin pairs were evaluated with the same techniques, but there were no statistically significant differences between affected and unaffected twins.     

Genetic and environmental risk factors for Parkinson's disease in a Chinese population

An epidemiological study of the environmental and geneticfactors as well as the possible interplay between them was conducted among 215 patients with Parkinson's disease and 313 controls in aChinese population in Hong Kong. In univariate analysis, a regular teadrinking habit was found to be a protective factor, which had not beenreported before. Smoking (a protective factor), family history,duration of pesticide exposure (in years) in farming and pesticideexposure during farming in women (both risk factors) have been reportedpreviously. In multivariate analysis, current smoking reachedborderline significance at the 5% level and the variables, yearsexposed to pesticides and family history were significant at the 10%level. By contrast with the common occurrence of polymorphism of theCYP2D6 gene (a gene involved with xenobiotic metabolism) in whitepeople, it is very rare in China and is not thought to be a significantfactor contributing to Parkinson's disease in Chinese people.

     

Genetic and environmental risk factors and their interactions for Parkinson's disease in a Chinese population.

The interaction between genetic and environmental factors for PD was examined in a Chinese population. It was found that although the intron 2 MAOB (GT)(n) repeat polymorphism was not associated with PD in the population, a relationship might have been masked by the "protective effect" of tea drinking. In individuals who did not drink tea (<1 cup/day), the possession of short length 相似文献   

Multiple risk factors for Parkinson's disease

OBJECTIVE: To determine the relative contribution of various risk factors to the development of Parkinson's disease (PD). METHODS: Ten variables that were independently associated with PD in a health system population-based case-control study of epidemiological risk factors for the disease were jointly assessed. Stepwise logistic regression, adjusted for sex, race and age was used to develop a multiple variate model that best predicted the presence of PD. The population attributable risk was estimated for each variable in the final model, as well as for all factors together. RESULTS: The 10 initial variables included >20 years occupational exposure to manganese or to copper, individually; >20 years joint occupational exposure to either lead and copper, copper and iron, or lead and iron; a positive family history of PD in first- or second-degree relatives; occupational exposure to insecticides or herbicides; occupational exposure to farming; and smoking. Logistic regression resulted in a final model that included >20 years joint occupational exposure to lead and copper (p=0.009; population attributable risk [PAR]=3.9%), occupational exposure to insecticides (p=0.002; PAR=8.1%), a positive family history of PD in first- and second-degree relatives (p=0.001; PAR=12.4%), and smoking 相似文献   

Familial and environmental risk factors in Parkinson's disease: a case-control study in north-east Italy

BACKGROUND AND OBJECTIVE: The aetiology of Parkinson's disease remains unknown, although both genetic susceptibility and environmental factors are considered putative contributors to its origin. We performed a case-control study to investigate the association of familial and environmental risk factors with Parkinson's disease (PD). METHODS: We studied 136 patients with neurologist confirmed PD and 272 age- and sex-matched controls, affected by neurological diseases not related to PD. The risk of developing idiopathic PD associated with the following familial and environmental factors: positive family history of PD, positive family history of essential tremor (ET), age of mother at subject's birth, rural birth, rural living, well water use, farming as an occupation, exposure to pesticides, head tremor, exposure to general anaesthesia and to ionizing radiations, food restriction, concentration camp imprisonment and smoking has been assessed by using univariate and multivariate statistical techniques. RESULTS: In the conditional multiple logistic regression analysis, positive family history of PD (OR 41.7, 95% CI 12.2-142.5, P < 0.0001), positive family history of ET (OR 10.8, 95% CI 2.6-43.7, P < 0.0001), age of mother at subject's birth (OR 2.6, 95% CI 1.4-3.7, P=0.0013), exposure to general anaesthesia (OR 2.2, 95% CI 1.3-3.8, P=0.0024), farming as an occupation (OR 7.7, 95% CI 1.4-44.1, P=0.0212) and well water use (OR 2.0, 95% CI 1.1-3.6, P=0.0308) exhibited a significant positive association with PD, whereas smoking showed a trend toward an inverse relationship with PD (OR 0.7, 95% CI 0.4-1.1, P < 0.06). CONCLUSIONS: We conclude that both familial and environmental factors may contribute to PD aetiology.     

Lifestyle-related risk factors for Parkinson's disease: a population-based study

OBJECTIVES: To investigate the association of major lifestyle-related risk factors with the prevalent cases of Parkinson's disease (PD) identified by the Italian Longitudinal Study on Aging. METHODS: A total of 5632 individuals randomly selected from the population registers of eight centers were screened for parkinsonism using both a questionnaire and a neurologic examination. Screened positives underwent a structured clinical work-up for the diagnosis of parkinsonism and parkinsonism subtypes. RESULTS: We identified 113 prevalent cases of PD. Age, male gender, and pesticide-use license were significantly related to PD. Heavy smoking was inversely related to PD. Age (OR = 1.1; 95% CI, 1.06-1.15) and pesticide-use license (OR = 3.7; 95% CI, 1.6-8.6) kept their significant correlation with the disease in the multivariate analysis to adjust for all the variables under investigation. Multivariate analyses were made for men and women separately: pesticide exposure was positively associated with PD only in men. CONCLUSIONS: Pesticide exposure might represent a candidate for environmental factors involved in PD.     

Environmental risk factors in Parkinson's disease.

We studied the environmental risk factors of Parkinson's disease (PD) in Finland, particularly those related to rural environment, in a prevalence material in 1992. The population numbered 196,864 people, including urban and rural areas. In this community-based study, we used a case-control method with personal investigation of the case subjects (n = 123) and matched control subjects (n = 246). Analyses were carried out by conditional logistic regression model. Case subjects had far fewer domestic animals at home during their lifetime, including cows, sheep, pigs, and chickens. The difference was even more obvious in those under the age of 20 years, including also cats and horses, but diminished after 20 years. The number of different animal species was smaller with case subjects as was the duration of animal contacts. Case subjects found their work physically heavier and exercised more. The mean age at onset in ever-smoking men was significantly higher than in never-smoking men. No special reason for non-smoking increased, and a physical reason decreased the risk of PD. Area of birth or living, farming and other occupations, types of drinking water, pesticide and herbicide use, head injuries, use of alcohol, education, and carbon monoxide poisonings were similar among case subjects and control subjects. In conclusion, domestic animals, or something that is connected with the animals, may have a protecting effect against PD. Alternatively, the observed negative associations of domestic animals at home and subsequent PD may only be a marker of other environmental conditions or lifestyles.     

Genetic and environmental factors of Parkinson's disease

We present a review on the genetic and environmental factors implicated in the aetiology of Parkinson's disease. The environmental hypothesis was strongly suggested about 20 years ago after the report of a parkinsonian syndrome in young adults that were intoxicated by a neurotoxin called MPTP which selectively destroys nigrostriatal dopaminergic neurons. Several chemical products used in herbicides and pesticides are similar structurally to MPTP, including paraquat, diquat and rotenone. Epidemiological studies have revealed an increased risk for Parkinson's disease with the use of pesticides and herbicides or the consumption of well water in rural areas of industrialised countries. However, it has not been possible to identify any causative environmental chemical agent in the aetiology of Parkinson's disease despite intensive research. Comparatively, the genetic hypothesis of Parkinson's disease has gained considerable interest during the last decade. Epidemiological studies reveal a family history in 10-25 p. cent Parkinson's disease patients. Several large kindreds with autosomal dominant Parkinson's disease associated with mutations of alpha-synuclein gene (PARK 1) were recently described. alpha-synuclein is a constituant of Lewy bodies, the hallmark of idiopathic Parkinson's disease. However, alpha-synuclein gene mutations are rare as opposed to parkin gene mutations (PARK 2), which are frequently found in autosomal recessive and sporadic young onset Parkinson's disease patients. Other genes or locus are implicated in autosomal dominant familial cases (PARK 3, 4 and 5). Nevertheless, a pure genetic origin can be demonstrated only in a minority of Parkinson's disease patients. Investigation of the possible interaction between genes and environment and of several candidate genes gave contradictory results, notably concerning the association between allelic variants of CYP2D6 gene and the occurrence of Parkinson's disease. In conclusion, the aetiology of Parkinson's disease remains unknown. There are probably several types or causes of Parkinson's disease. In most cases, this heterogeneity could be attributed both to genetic and environmental factors.     

Follow-up study of early-life protective and risk factors in Parkinson's disease

Previous studies suggest that Parkinson's disease (PD) is negatively associated with early-life intake of vitamin E-rich foods and positively associated with rural experience. Using a new survey design, we attempted to confirm and extend these results. We gave a telephone questionnaire to 106 patients with PD and to their spouses as controls. It assessed premarital consumption of 31 foods of various vitamin E content, vitamin supplements, and exposure to rural living. Respondents rated food consumption with respect to what they perceived as the average for their sex and age at that time. We found female patients with PD less likely than spouses to have eaten "peanuts and peanut butter" (p less than .05), which are high in vitamin E. "Salad with dressing," also high in vitamin E, gave a similar result (p less than .05) for a male-predominant patient group. Separate comparison of male controls with female controls ruled out sex-related preferences as the explanation of our findings. Patients had more extensive rural experience and were more likely to have frequently sprayed pesticides (p less than .05) than had controls. Our results justify further investigations into early-life vitamin E intake, pesticides, and neurotoxins associated with rural life.     

Parkinson's disease and environmental factors. Matched case-control study in the Limousin region, France

The study included 140 patients with Parkinson's disease (PD) and 280 non-Parkinson age-matched controls to evaluate environmental risk factors associated with PD. The effect of exposure to environmental and dietary factors was determined using conditional logistic regression. This multivariate analysis showed that PD in first-degree relatives and tea drinking were the main risk factors for PD. Smoking appeared to be a protective factor. Exposure to toxic compounds was not a significant risk factor. Further research is needed to validate that tea consumption increases the risk of PD.     

Environmental risk factors in Parkinson's disease

To investigate possible risk factors for Parkinson's disease (PD) we conducted a case-control study of 150 PD patients and 150 age- and sex-matched controls. We interviewed and examined all 300 subjects. We collected demographic data including lifetime histories of places of residence, source of drinking water, and occupations such as farming. Subjects completed a detailed questionnaire regarding herbicide/pesticide exposure. Rural living and drinking well water were significantly increased in the PD patients. This was observed regardless of age at disease onset. Drinking well water was dependent on rural living. There were no significant differences between cases and controls for farming or any measure of exposure to herbicides or pesticides. These data provide further evidence that an environmental toxin could be involved in the etiology of PD.     

Dyskinesia in Parkinson's disease. Pathophysiology and clinical risk factors

Development of dyskinesia is a common phenomenon during the long-term course of Parkinson's disease. During the last few years some but not all pathogenetic mechanisms causing dyskinesias in PD have been better understood. Severity of Parkinson's disease and levodopa dosing are the main clinical risk factors. Most concepts underline the significance of pulsatile D1-receptor stimulation for the development of dyskinesias. The interactions between D1- and D2-mediated STR-Gpi pathways and co-localized neuropeptides are important but not fully understood. Glutamatergic overactivity might also be a significant pathogenetic factor. According to these pathophysiological concepts, therapeutic strategies focus mainly on continuous postsynaptic DA-receptor stimulation by long acting DA agonists or highly selective D2 agonists. Another strategy is the use of NMDA antagonists.     

Dyskinesia in Parkinson's disease. Pathophysiology and clinical risk factors

Journal of Neurology - Development of dyskinesia is a common phenomenon during the long-term course of Parkinson's disease. During the last few years some but not all pathogenetic mechanisms...     

Cognitive-behavioral therapy for depression in Parkinson's disease: a pilot study.

The present study was conducted to examine the feasibility and effect of an individual cognitive-behavioral treatment (CBT) for depression that was modified to meet the unique needs of the PD patient and incorporated a separate social support intervention for caregivers. Fifteen PD patients with Major Depressive Disorder participated in the study with a caregiver. Patients received 10-14 sessions of modified individual CBT. Caregivers attended 3-4 psychoeducational sessions, occurring separately from the patients treatment sessions, which focused on strategies for offering appropriate support, and ways to respond to the patients' negative thoughts in a targeted manner. Patients experienced a significant reduction in depressive symptoms and negative cognitions, and an increased perception of social support over the course of treatment. Gains were maintained at 1-month follow-up. In conclusion, individual CBT, when modified appropriately, may be a feasible and effective option for PD depression. Larger, randomized controlled trials are needed to further evaluate the efficacy of this intervention and to identify specific mechanisms of change.     

Ethosuximide and tremor in Parkinson's disease: a pilot study.

Following the demonstration of an anti-tremor effect of ethosuximide in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkey model, we have tested the effect of this drug in 10 patients with typical parkinsonian tremor. Six patients suffered from Parkinson's disease with prominent, relatively drug-resistant rest tremor. The other four patients had a drug-induced parkinsonian tremor due to neuroleptic agents taken for a psychiatric condition. Five of the six parkinsonian patients and three of the four psychiatric patients reported within a few days a marked and intolerable exacerbation of their tremor. One patient in each group was improved, and this improvement was verified in repeated examinations. Thus, for unknown reasons, the effect of ethosuximide was not as predicted by the monkey model. Among possible explanations is the fact that we had chosen patients with drug-resistant tremor.