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.     

A family history of Parkinson's disease and its effect on other PD risk factors.

Parkinson's disease (PD) is likely a result of both inherited and exogenous factors. In a study of 144 PD cases and 464 controls, we used PD family history as a surrogate for inherited PD susceptibility. Cases were more likely to report a first- or second-degree relative with PD: 16.0 vs. 4.3%; odds ratio (OR) = 4. 2; 95% confidence interval (CI) = 2.3-7.6. A PD family history was a greater risk factor for PD in subjects under age 70 (OR = 8.8; 95% CI = 3.4-22.8) compared with those over 70 (OR = 2.8; 95% CI = 1.3-6. 1) and in men (OR = 8.1; 95% CI = 3.4-19.2) compared with women (OR = 2.6; 95% CI = 1.1-6.0). We also tested whether a PD family history modified the effects of other PD risk factors. In subjects with a PD family history, occupational exposure to copper, lead or iron increased the risk for PD (OR = 3.0; 95% CI = 0.7-13.3), but this was not the case for those without a family history (OR = 1.1; 95% CI = 0.7-1.6). Ever smoking cigarettes was inversely associated with PD in those without a PD family history (OR = 0.6; 95% CI = 0.4-0.9), but was positively associated with PD in those with a PD family history (OR = 1.7; 95% CI = 0.5-5.9). In summary, our results suggest that a PD family history, and perhaps, therefore, an inherited susceptibility, confers a greater risk for PD in men and individuals under 70 years of age and may modify the effects of environmental risk factors for PD.     

Familial aggregation of Parkinson's disease: a population-based case-control study in Europe. EUROPARKINSON Study Group.

OBJECTIVE: To investigate the familial aggregation of PD in a large collaborative population-based case-control study. BACKGROUND: Most previous case-control studies of the familial aggregation of PD have been hospital- or clinic-based. METHODS: We included 219 prevalent cases ascertained in three European populations (centers), using a two-phase design consisting of screening and examination by a neurologist. Each case was matched by age, sex, and center to three controls drawn from the same populations (n = 657). Presence of PD among first-degree relatives (parents and siblings) was determined using the family history approach for 175 cases and 481 controls. RESULTS: Overall, a positive family history (at least one parent or sibling affected by PD) was reported in 10.3% of patients and 3.5% of controls (odds ratio [OR] = 3.2; 95% confidence interval [CI] = 1.6 to 6.6). A similar association was observed when analyses were restricted to nondemented patients and controls (OR = 3.9; 95% CI = 1.7 to 8.7) or to newly diagnosed patients (OR = 3.3; 95% CI = 0.9 to 11.9). We found a significant trend of increasing risk with increasing number of affected relatives (p = 0.003). Analyses stratified by age showed a stronger association for younger PD patients (OR = 7.6; 95% CI = 1.5 to 38.9) than for older patients (OR = 2.5; 95% CI = 1.1 to 5.7). CONCLUSIONS: In this large sample of prevalent PD patients and population-matched controls, PD significantly aggregates in families, with the strength of the association being age-dependent. Therefore, familial factors, which can be genetic, environmental, or both, play a role in PD.     

Evidence of shared risk for Alzheimer’s disease and Parkinson’s disease using family history

This case-control study examined the potential for a common etiology of Parkinson’s disease (PD) and Alzheimer’s disease (AD) using reported family history. Structured interviews were used to collect AD and PD family history from subjects (n = 1531) with AD, PD, AD/PD, or controls. Intergroup analysis compared reported AD and PD family histories in the three case groups to the histories reported in the control group. Intragroup analysis stratified each diagnostic group based on positive family history of AD, then compared the subgroups for a family history of PD. Subjects with AD had a higher risk of having a family history of AD [odds ratio (OR) 2.3; 1.5–3.4] and subjects with PD had a higher risk of having a family history of PD (OR 2.2; 1.2–4.0) as compared to control subjects. Intergroup analyses revealed no significant crossed risk, increased risk of subjects with AD having a family history of PD vs controls and vice versa. Intragroup analysis found that subjects with PD and a family history of AD were more likely to have a family history of PD (OR 1.7; 1.1–2.6) when compared to subjects with PD and no family history of AD. A similar trend was found for subjects with AD (OR 1.7; 0.9–3.1). AD and PD cases each have an increased familial risk of their respective disease. Probands with AD or PD and a family history of either disease have a higher crossed risk of a family history of the other disease. These findings suggest the existence of common genetic and/or environmental factors that predispose to both AD and PD in the subset of cases with positive family history of both neurodegenerative diseases.     

帕金森病与饮茶的病例对照研究

目的探讨饮茶同原发性帕金森病(PD)的关系。方法采用以人群为基础的病例对照研究,调查在北京地区55岁以上PD患病率调查中确诊及2002年8月至2003年1月在北京协和医院帕金森研究中心诊治的病人共114例;以及性别、民族及居住地与其匹配的对照205例。采用统一的危险因素结构式问卷和诊断标准对所有对象的社会人口学资料和个人的生活习惯:饮茶、吸烟、饮酒及一级亲属的家族史因素与PD发病情况进行调查,应用单因素和多因素分析方法对有关因素进行分析。结果在饮茶与PD关系的单因素分析中,以非饮茶人群为对照,饮茶者患PD的比值比(OR)为0.23(95%CI:0.14,0.62;P<0.01)。经多因素的非条件Logistic回归分析后,饮茶者的OR值为0.199(95%CI:0.114,0.345;P<0.001)。结论北京地区居民中饮茶与帕金森病呈显著负相关联,为PD的保护性因素。     

Case-control study of multiple system atrophy.

The epidemiology of multiple system atrophy (MSA) is scarcely known, and risk factors have not been definitely identified. We investigated the effect of family history for neurodegenerative diseases and environmental factors on MSA risk in a multicentric case-control study. A total of 73 MSA patients (42 men, 31 women; age, 64.3 +/- 8.1 years; disease duration, 4.8 +/- 3.9 years), 146 hospital controls (84 men, 62 women; age, 64.9 +/- 8.4 years), and 73 population controls (42 men, 31 women; age, 63.7 +/- 8.9 years) matched for sex, age (+/-3 years), and province of residence were enrolled consecutively at seven neurological centers from 1 January 1994 to 31 July 1998. The following variables were investigated: family history of neurodegenerative diseases, education, smoking habits, hobbies, and occupational history. Occupational history of farming was significantly more frequent among MSA cases than controls (OR adj = 2.52; 95% CI, 1.25 to 5.07, MSA vs. hospital controls; OR adj = 4.53; 95% CI, 1.68 to12.2, MSA cases vs. population controls). A dose-response analysis for years of farming corroborated this association. We recently found that smoking is significantly less frequent among MSA cases than controls (Vanacore et al. [2000] Neurology 54:114-119). Here, we report that the effects of farming and smoking on MSA risk do not interact. Our results suggest that occupational history of farming is a risk factor for MSA. Smoking and farming seem to influence MSA risk independently. Further epidemiological studies might provide clues on the etiopathogenesis of MSA.     

Risk factors for Parkinson disease and the path analysis： One-to-one paired design

BACKGROUND： Parkinson disease （PD） results from the reduce of neurotransmitter dopamine that transmits intracellular information in brain caused by some reasons, then leads to the dynamic disequilibrium with another neurotransmitter of acetylcholine which is relatively hyperactive. The main causes for PD are still unclear. OBJECTIVE： To screen out the risk factors of PD by means of univariate analysis and multivariate Logistic regression analysis, and investigate the manner of actions between various factors and PD, so as to provide clues for the etiological study of PD. DESIGN： A paired design, Logistic regression analysis, path analysis. SETTING： Department of Scientific Research, Shandong Institute of Physical Education. PARTICIPANTS： Totally 157 PD patients were selected from the Department of Neurology, Qilu Hospital of Shandong University from November 2001 to October 2002. Inclusive criteria： PD was diagnosed according to the standard set by the Fourth National Seminar on Extrapyramidal Disease, Parkinsonian syndromes caused by stroke, carbon monoxide poisoning, encephalitis, drugs, etc. were excluded. Another 157 patients treated in the same department at the same period were selected as the control group, they were the same in sex as those in the patient group, within 3 years older or younger than those in the patient group, and without PD or other extrapyramidal diseases. METHODS： （1） The general conditions were investigated in all the subjects, including general conditions, social behavioral factor, environmental factor, genetic factor, life events, and previous disease; There were 12 main variables, including educational level, family history, mental labour, contact to insecticides, living place before school-age, smoking index, drinking index, tea-drinking index, history of brain trauma, history of cardiovascular disease, history of diabetes mellitus, and history of depression. （2） SAS6.12 software and SPSS 10.0 software were used in the conditional Logistic regression analysis and path analysis respectively. MAIN OUTCOME MEASURES： The results of 12-variable univariate and multivariate analyses; Correlation between main variables and PD; Effects of the factors. RESULTS： All the subjects were involved in the analysis of results. （1） The results of Logistic regression analysis showed that family history, mental labour, insecticides, drinking index and history of depression all had significant positive correlations with PD （univariate analysis： OR=1.405- 5.429, P 〈 0.05- 0.01; multivariate analysis： OR=2.029- 6.754, P 〈 0.05- 0.01）, whereas smoking had significant negative correlations with PD [univariate analysis： odd ratio （OR）=0.765, P 〈 0.05; multivariate analysis： OR =0.489, P 〈 0.01]. （2） The path analysis showed that family history, mental labour, insecticides, smoking, drinking and history of depression had direct effects on PD occurrence [（path coefficient= - 0.218 to 0.204, P 〈 0.05 -0.01）]; Insecticides could cause PD indirectly on the basis of family history （genetic susceptibility） （path coefficient=0.946, P 〈 0.01）; Insecticides could also cause PD by drinking （path coefficient=0.165, P 〈 0.01） Drinking could cause PD indirectly on the basis of family history （path coefficient=0.043, P 〈 0.01 ）. CONCLUSION： The main risk factors of PD are family history, history of depression, drinking, mental labour and insecticides, whereas the protective factor is smoking. PD attack has genetic susceptibility, insecticides and drinking can cause PD on the basis of PD family history. The risk of PD can be decreased by reducing the occasion for contacting the environmental risk factors.     

Interactions between four gene polymorphisms and their association with patients with Parkinson's disease in a Chinese Han population

The four previously reported Parkinson's disease (PD)-related single-nucleotide polymorphisms (SNPs) – rs1775143, rs823114, rs2071746 and rs62063857 – have rarely been studied in Chinese Han populations. To examine the association between these SNPs and PD, we conducted a case-control study of 158 patients with PD and 210 controls. All participants were Chinese Han from Northern China. With covariate adjustment for clinical characteristics, logistic regression analysis revealed no differences in genotype or allele frequencies for the four SNPs. Stratified by age of disease onset, sex, smoking status, duration of disease, baseline UPDRS, Hoehn–Yahr Stage, PD subtypes, scores of Hamilton anxiety scale, Hamilton depression scale and activity of daily living, all of the p values did not remain significant after Bonferroni correction. However, the haplotype rs1775143T-rs823114G-rs2071746T-rs62063857A was associated with increased risk of developing PD (p = 0.003, OR = 456.88, 95% CI: 27.40–7619.75) in our case-control sample set. The haplotype rs1775143T-rs823114G-rs2071746T was also associated with increased risk of developing PD (p = 0.003, OR = 338.43, 95% CI: 20.68–5538.27). Although the haplotype rs1775143T-rs823114G-rs62063857A was associated with increased risk of PD (p = 0.03), the 95% CI was 0.993–22.469. Our data demonstrate that although specific SNPs were not related with PD patients, certain haplotypes were associated with increased risk for PD in the Chinese Han population. These results provide further evidence that the etiology of PD is multifactorial, although the underling mechanism needs further study.     

Familial occurrence of Parkinson's disease in a community-based case-control study

Purpose: To study the occurrence of Parkinson's disease (PD) in the relatives of parkinsonian patients (n=119), and of their matched controls (n=238).

Scope: More patients reported a positive family history of PD in their first degree relatives, compared to their controls (OR 2.7, 95% CI 1.3–5.9), and the incidence of PD among those relatives was also significantly higher (OR 1.4, 95% CI 1.1–1.8).

Conclusions: Familial occurrence of PD is not necessarily a sign of genetic mechanisms in the etiology of PD. Shared environment with common risk factors might be even more important.     

Parkinson''s disease, smoking and family history: meta-analysis

To estimate the pooled risk of tobacco smoking for Parkinson's disease (PD) in patients with and without PD family history. We conducted systematic searches of Medline, PsycLIT, Embase, Current contents, Best Evidence, Nisc Mexico Biblioline, previous reviews, examination of cited reference sources and personal contact and discussion with several investigators expert in the field. Studies in all languages were considered. Published observational studies on PD and cigarette smoking stratified by PD family history were reviewed. When two or more papers were based on an identical study, the paper that principally investigated the relationship between PD, smoking stratified by PD family history or the paper that was published last was used. Three case-control studies were carried out between 1996 and 2000, of which one reported risk estimates. The risk of ever smoker in patients with positive PD family history was 0.82 (95% confidence interval 0.44-1.53). There was an obvious protective effect in the pooled estimate in patients with negative PD family history [odds ratio 0.77 (95% confidence interval 0.59-1.01)]. Although our pooled estimates show that smoking is inversely associated with the risk of PD only in patients with negative PD family history, further studies evaluating the interaction between smoking and PD family history are strongly needed.     

Occupations and Parkinson's disease: a multi-center case-control study in South Korea

OBJECTIVE: We performed a hospital based case-control study in South Korea (1) to clarify the role of occupational exposure, and especially manganese (Mn) exposure in the etiology of Parkinson's disease (PD) and (2) to discover the association between any occupations and PD. METHODS: We selected two groups, PD patient group (N1) and controls (N2). Three hundred sixty-seven consecutive outpatients with PD (177 men, 190 women) and 309 controls were interviewed about life style, past history, family history, education level, and occupational history etc. We employed a range of industrial categories as defined by section (the most broad category) and division (sub-category) of the Korea Standard Industry Code (KSIC) Manual. Along with KSIC, we also used the Korea Standard Classification of Occupations (KSCO) as proxies of occupational exposure. The odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for age, sex, smoking status, and education level are presented. RESULTS: As regarding the exposure to hazardous materials, especially Mn, more subjects in the control group than the PD patient group have worked in the occupations with potential exposure to Mn (P < 0.001). Ever having worked in 'agriculture, hunting, and forestry' section of industry was positively associated with PD (OR 1.88), and 'agriculture production crops (OR 1.96)' division of industry was positively associated with PD. On the other hand, ever having worked in the 'manufacturing (OR 0.56)', 'transportation (OR 0.28)' section of industry, and 'transporting (OR 0.20)' division of industry were negatively associated with PD. 'Drivers (OR 0.13)' division of occupation also was negatively associated with PD. CONCLUSIONS: To our knowledge, this is the first case-control studies to find an inverse relationship between 'transporting' or 'technicians like machinery engineers' as his/her longest job and PD risk. Because of this unexpected finding, our work should be replicated in various populations.     

Active and passive cigarette smoking and risk of intracranial meningioma

Motivated by prior studies, we examined associations between cigarette smoking and risk of intracranial meningioma in a population-based case-control study, including 200 cases and 2 controls matched to each case on age and sex. Subjects were asked to recall their history of active and passive cigarette smoking occurring 10 or more years before the date of meningioma surgery. Ever active smoking was associated with an increased risk of meningioma in men (OR = 2.1; 95% CI 1.1-4.2) but not in women (OR = 0.7; 95% CI 0.5-1.1). The statistical interaction by gender was significant (p = 0.01). In men, risk increased with increasing number of cigarettes smoked daily (p for trend = 0.04). In women, the trend was opposite (p for trend = 0.08). Among never active smokers, passive smoking from a spouse was associated with increased risk in both sexes (OR 2.0; 95% CI 1.1-3.5), and risk increased with increasing duration of exposure (p for trend = 0.02). Uncertain is whether these findings reflect a true biological phenomenon or result from chance or uncontrolled confounding.     

Dose-dependent protective effect of coffee, tea, and smoking in Parkinson's disease: a study in ethnic Chinese

INTRODUCTION: Few studies have examined the relationship of coffee and tea in Parkinson's disease (PD). The potential protective effect of coffee intake and risk of PD has not been studied in a Chinese population. There is a high prevalence of caffeine takers among Chinese in our population. OBJECTIVE: We undertook a case control study to examine the relationship between coffee and tea drinking, cigarette smoking, and other enviromental factors and risk of PD among ethnic Chinese in our population. METHODS AND RESULTS: 300 PD and 500 population controls were initially screened. Two hundred case control pairs matched for age, gender, and race were finally included in the analysis. Univariate analysis revealed significant association of PD with coffee drinking (p<0.0005), tea drinking (p=0.019), alcohol drinking (p=0.001), cigarette smoking (p<0.0005), and exposure to heavy metals (p=0.006). Conditional logistic regression analysis demonstrated that amount of coffee drunk (OR 0.787, 95%CI 0.664-0.932, p=0.006), amount of tea drunk (OR 0.724, 95%CI 0.559-0.937, p=0.014), number of cigarettes smoked (OR 0.384, 95%CI 0.204-0.722, p=0.003), history of heavy metal and toxin exposure (OR 11.837, 95%CI 1.075-130.366, p=0.044), and heart disease (OR 5.518, 95%CI 1.377-22.116, p=0.016) to be significant factors associated with PD. One unit of coffee and tea (3 cups/day for 10 years) would lead to a 22% and 28% risk reduction of PD. One unit of cigarette smoke (3 packs/day for 10 years) reduced the risk of PD by 62%. CONCLUSIONS: We demonstrated a dose-dependent protective effect of PD in coffee and tea drinkers and smokers in an ethnic Chinese population. A history of exposure to heavy metals increased the risk of PD, supporting the multifactorial etiologies of the disease.     

Occupational exposure to manganese, copper, lead, iron, mercury and zinc and the risk of Parkinson's disease.

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.     

Nonsteroidal anti-inflammatory drugs and risk of Parkinson's disease.

Inflammation and oxidative stress have been implicated as pathogenic mechanisms in Parkinson's disease (PD). Evidence from in vitro and animal studies suggests a possible protective role of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. We investigated the risk of PD associated with use of aspirin and nonaspirin NSAIDs in a population-based case-control study among enrollees of Group Health Cooperative, a health maintenance organization in the Seattle area. Subjects included 206 cases between ages 35 and 89 with a new diagnosis of idiopathic PD between 1992 and 2002, and 383 randomly selected controls frequency-matched by age, sex, duration of enrollment, and clinic. We obtained information on participants' age, smoking, and medical history from interview. Exposure to NSAIDs was ascertained from an automated pharmacy database. Medications filled within 5 years of the interview were excluded. After adjusting for age, sex, smoking, duration of enrollment, and clinic, the risk of PD among individuals who received nonaspirin NSAIDs between 1977 and 1992 was 0.90 (95% CI: 0.59-1.35) and 1.67 (95% CI: 0.60-4.60) between 1993 and 2002. Use of ibuprofen was not associated with PD (OR: 0.89; 95% CI: 0.60-1.32). The risk of PD associated with aspirin or aspirin-containing medications was 0.74 (95% CI: 0.49-1.12). We observed no trend in risk according to number of fills for these drugs. Our results provide only limited support for the hypothesis that use of aspirin may reduce the risk of this disease, and no indication of protection from other NSAIDs.     

Differential effect of environmental risk factors on postural instability gait difficulties and tremor dominant Parkinson's disease

Both environmental and genetic factors contribute to the development of Parkinson's disease (PD). We have examined environmental risk factors in a Norwegian population of incident PD patients and controls, the Norwegian ParkWest study. All five neurological wards in the study area of Western Norway participated in the study. A 4‐step diagnostic procedure was used to establish a representative cohort of patients with incident PD at a high level of diagnostic accuracy. 212 incident PD patients and 175 age‐ and gender‐matched controls were included. PD patients and controls were asked for information on occupation, education, exposure to pesticides, tobacco, alcohol, and caffeine. Agricultural work was associated with a higher risk of PD (OR 1.75 (1.03–3.0) P = 0.009). There were no differences as to other occupations. Smoking (OR 0.63 (0.42–0.95) P = 0.016) and alcohol use (OR 0.55 P = 0.008) were associated with a lower risk for PD. Interestingly, this inverse association was only seen in postural instability gait difficulties (PIGD) PD (P = 0.046 for smoking, P = 0.07 for alcohol consumption), and not in tremor dominant (TD) PD which was similar to controls. Consumption of coffee was lower in PD patients (3.3 ± 1.8 cups per day vs. 3.8 ± 2.0 in controls P = 0.02). In the regression model including intake of alcohol, coffee, and smoke, only coffee (P = 0.007) and alcohol intake (P = 0.021) remained significant whereas smoking was no longer significant. Thus, it seems as though only coffee intake reduces the risk of PD in general while associations to alcohol and smoking differ between PIGD and TD‐PD patients. © 2010 Movement Disorder Society     

Risk factors for cryptogenic and idiopathic partial epilepsy: a community-based case-control study in Copparo,Italy

OBJECTIVES: The etiology of epilepsy remains unknown in most cases. We sought to investigate the role of some pre-, peri- and postnatal factors in the etiology of idiopathic and cryptogenetic partial epilepsy. METHODS: We carried out a community-based case-control study using the incidence cohort of epileptic patients living in the district of Copparo, in the province of Ferrara, Italy. The study was performed in 55 cases and 165 controls. A standardized questionnaire was used to collect information in face-to-face interviews. RESULTS: Multivariate logistic regression analysis found that a personal history of febrile convulsions [odds ratio (OR) = 4.01, 95% confidence interval (CI) = 1.3-19.1] and a family history of seizures in first-degree relatives (OR = 4.5, 95% CI = 1.8-18.6) were independent risk factors for the condition under study. We failed to demonstrate an association between partial epilepsy and previously suggested perinatal risk factors. CONCLUSION: The findings of this study further support the hypothesis of a genetic propensity for seizures, which may be expressed early by the occurrence of febrile convulsions.     

赤峰市脑卒中危险因素的城乡差异研究

目的 探讨赤峰市居民脑卒中危险因素的城乡差异.方法 利用整群抽样方法抽取赤峰市≥40岁常驻人口 18835名.收集临床资料,并对结果进行统计分析.结果 城镇居民及乡村居民前三位危险因素均为缺乏运动、高血压病及超重或肥胖.与乡村居民比较,城镇居民脑卒中家族史、高血压病、糖尿病、超重或肥胖、卒中既往史、血脂异常的暴露率显著...     

Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia.

The epsilon4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one epsilon4 allele (OR=3.37; P=0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one epsilon4 allele (59.7 years) as compared with those homozygous for the more common epsilon3 allele (62.4 years; P=0.009). Thus, consistent with previous studies, we find evidence that the presence of an epsilon4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology.