Parkinson's disease seems to occur more commonly in men than women based primarily on studies of death rates and prevalence. In recent years, several population based incidence studies of Parkinson's disease that included sex data have been conducted in a variety of populations around the world. To investigate whether these incidence studies suggest an increased risk of Parkinson's disease in men, a meta-analysis was performed of the differences in incidence of Parkinson's disease between men and women reported in seven studies that met the inclusion criteria. A significantly higher incidence rate of Parkinson's disease was found among men with the relative risk being 1.5 times greater in men than women. Possible reasons for this increased risk of Parkinson's disease in men are toxicant exposure, head trauma, neuroprotection by oestrogen, mitochondrial dysfunction, or X linkage of genetic risk factors. Whether there is a sex difference in risk for Parkinson's disease (PD) is controversial.1 PD seems to occur more commonly in men than women based primarily on studies of death rates and prevalence. 1 2 Death rates, however, do not accurately reflect the incidence of PD 3 because of inaccurate diagnoses on death certificates. Likewise, prevalence data are problematic. Prevalence studies are subject to potential sex differences in survival, access to health care, access to the system whereby cases were ascertained for inclusion in the study, and sex differences in the underlying population. 1Because incidence of PD represents the number of new cases developed or diagnosed during a specific time interval within a predefined population at risk, incidence measurements are more direct and unambiguous epidemiological estimates of risk for developing PD than are death rates or prevalence. Incidence data from well defined populations obviate a number of concerns with prevalence data, such as differential mortality between men and women.In recent years, several population based incidence studies of PD that included sex data have been conducted in a variety of populations around the world. To determine whether these incidence studies suggest an increased risk of PD in men, we performed a meta-analysis of the differences in incidence of PD between men and women reported in these studies. METHODSThe Medline database was searched for population based ascertainment studies of PD average annual incidence rates adjusted for sex and age. The studies included in our metaanalysis met six criteria: (1) The study must have been published after 1980. Inclusion of studies published before 1980 would lead to the inclusion of neurodegenerative disorders that would be recognised now as not being PD (for example, progressive supranuclear palsy, multiple system atrophy, etc). Also, older studies are more likely to be contaminated with cases of post-encephalitic parkinsonism than studies published after 1980; (2) studies must have excluded secondary and/or drug induced parkinsonism; (3) studies must have ascertained at least 50 cases of PD; (4...

Background: Although estrogen therapy has been associated with improved cognitive functioning, a reduced risk of dementia in women with Parkinson disease (PD), and a decreased risk of Alzheimer disease, estrogen therapy has not affected the risk of PD per se. Objective: To determine whether postmenopausal women with PD differed from control subjects with regard to estrogen exposure. Design, Setting, and Patients: A case-control design was used, abstracting questionnaire data obtained via interview from 133 female PD cases and 128 female controls duringroutineoutpatientclinicvisitsin1999atamid-Atlantic tertiary care referral center. There were 140 subjects (68 PD cases and 72 controls) who met the inclusion criteria. Main Outcome Measure: Use of postmenopausal estrogen therapy. Results: More women in the control group than in the PD group took postmenopausal estrogen (36 [50%] of 72 women vs 17 [25%] of 68 women; PϽ.003), and women who had taken postmenopausal estrogen were less likely to develop PD than those who had not (odds ratio, 0.40 [95% confidence interval, 0.19-0.84]; PϽ.02). Among PD cases only, postmenopausal estrogen use was not associated with age of onset. Conclusion: Postmenopausal estrogen therapy may be associated with a reduced risk of PD in women.

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Dopamine D(1) agonists can induce a full antiparkinsonian response but do not support previous hypotheses suggesting that D(1) agonists are more or less likely to produce dyskinesias than levodopa.

Recent data suggesting complex I dysfunction in Parkinson's disease (PD) arises from mitochondrial DNA (mtDNA) mutation does not conclusively answer whether the responsible genetic lesion is inherited (primary) or somatic (secondary). To address this question, we identified a family in which multiple members over three generations are affected with PD through exclusively maternal lines. Cytoplasmic hybrids (cybrids) were created for 15 family members over two generations by transferring each individual's mtDNA to mtDNA-depleted human neuroblastoma cells. Eight of the 15 cybrid lines contained mtDNA obtained from maternally descended family members and seven contained mtDNA from paternally descended family members. After 6 weeks of culture, cybrid cell lines were assayed for complex I activity and oxidative stress, and mitochondrial morphology was analyzed by electron microscopy. Compared with the cybrid lines containing mtDNA from paternal descendants, cybrid lines containing mtDNA from maternal descendants had lower complex I activity, increased reactive oxygen species production, increased radical scavenging enzyme activities, and more abnormal mitochondrial morphologic features. These findings were present in cybrid lines containing mtDNA from maternal descendants with PD as well as in currently asymptomatic young maternal descendants, and support a precedent for inherited mtDNA mutation in some persons with PD.