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)

The relationship between trauma and the development of Parkinson's disease has been an issue in neurology since James Parkinson's initial 1817 essay. This paper will delineate the historical development of the concept of trauma as an etiologic agent in Parkinson's disease and parkinsonism. The strong influence of socioeconomic societal forces in the 1870s with regard to liability laws and the subsequent acceptance in the medical community of the role of peripheral trauma in producing Parkinson's disease is presented. We will also review present-day criteria for assigning head trauma an etiologic role in parkinsonism. The discussion will stress current knowledge regarding trauma and parkinsonism, and it will also review the issues of the possible role of the current litigious society's influence on determining a role for trauma in Parkinson's disease.
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PMID:Trauma as an etiology of parkinsonism: a historical review of the concept. 267 2

This article reviews evidence for the occurrence of atypical parkinsonism in Afro-Caribbean and Indian ethnic minority subjects living in western countries, particularly the UK. Current information on the frequency, pattern, and prevalence of Parkinson's disease and parkinsonism in these communities is unclear and controversial. While several workers have suggested that there is a low prevalence of Parkinson's disease in populations of African origin, other workers have suggested a higher prevalence of Parkinson's disease in African Americans. Furthermore, little information is available in relation to the pattern of parkinsonism in these subjects. A recent phenomenologic study of parkinsonism in the French West Indies by Caparros-Lefebvre and colleagues has indicated a significantly increased frequency of atypical parkinsonism in local non-white subjects. Since 1995, we have been studying the pattern and frequency of parkinsonism in Afro-Caribbean and Indian (originating from the Indian subcontinent) patients living in the UK, with London serving as the coordinating center. Our results indicate that there is a three- to fourfold increase in the frequency of occurrence of sporadic atypical parkinsonism characterized by levodopa hyporesponsiveness, bradykinesia-dominant disease, and early cognitive dysfunction in these patients even after exclusion of patients with clinically probable multiple system atrophy, progressive supranuclear palsy, and Lewy body dementia. These findings are similar to observations made in the French West Indies. Ongoing studies in India suggest that atypical parkinsonism also affects local patients, and the pattern of parkinsonism tends to differ from Afro-Caribbean subjects in the UK. Studies are currently underway to unravel the mechanism of increased frequency of atypical parkinsonism in these ethnic groups and include genetic studies addressing polymorphisms of enzymes metabolizing levodopa, dietary neurotoxin screen and functional imaging studies of the striatum using positron emission tomography. Furthermore, the contribution of diabetes mellitus and hypertension, commonly seen in these ethnic groups, is also being examined.
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PMID:Atypical parkinsonism in Afro-Caribbean and Indian origin immigrants to the UK. 1063 37

In contrast to Alzheimer's disease, effective therapeutic options are available for Parkinson's disease. Therapy of dopamine replacement such as levodopa improves the symptoms of this disease, but does not inhibit neurodegeneration in the substantia nigra. Numerous studies have suggested that endogenous and environmental neurotoxins, and oxidative stress may participate in this disease, but the detailed mechanisms are still unclear. Recent genetic studies in familial Parkinson's disease and parkinsonism show several gene mutations. This new information regarding pathogenesis offers novel prospects for therapy. To develop novel neuroprotective drugs, it is necessary to have a model for each type of parkinsonism. This review summarizes current findings regarding parkinsonian models in vertebrates and invertebrates and discusses their value.
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PMID:The parkinsonian models: invertebrates to mammals. 1113 23

In Parkinson's disease, while dopamine (DA) replacement therapy, such as with L-DOPA (levodopa), improves the symptoms, it does not inhibit the degeneration of DA neurons in the substantia nigra. Numerous studies have suggested that both endogenous and environmental neurotoxins and oxidative stress may participate in this disease, but the detailed mechanisms are still unclear. Recent genetic studies in familial Parkinson's disease and parkinsonism have shown several gene mutations. This new information regarding its pathogenesis offers novel prospects for effective strategies involving the neuroprotection of vulnerable DA neurons. This review summarizes current findings regarding the pathogenesis and antiparkinsonian drugs, and discusses their possibilities of targets to develop novel neuroprotective drugs.
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PMID:Antiparkinsonian drugs and their neuroprotective effects. 1191 20

Administrative databases have the potential to assess quality and cost of care for parkinsonism and Parkinson's disease. However, the validity of findings is limited by our understanding of how cases are identified. Patient records listing International Classification of Diseases, Version 9, Clinical Modification (ICD-9 CM) codes for parkinsonism (n = 2,076) and dopaminergic medications (n = 2,798) were pulled from fiscal years 1999 to 2001 for patients in the Pacific Northwest Veterans Administration. Samples of these records (n = 397) and records without these ICD-9 CM codes (n = 500) were reviewed, and clinical data were extracted. The accuracy of administrative data to identify and distinguish between Parkinson's disease and parkinsonism was calculated. A total of 37.9% of parkinsonism cases were detected using pharmacy data and ICD-9 CM codes compared to 18.7% by using ICD-9 CM codes alone. The ICD-9 CM code for paralysis agitans (332.0) did not distinguish between probable Parkinson's disease and other causes of parkinsonism, whereas the ICD-9 CM code for degenerative basal ganglia disorder (333.0) predicted having secondary parkinsonism (odds ratio [OR] = 5.0) as well as dopa-responsiveness in patients without secondary parkinsonism (OR = 4.5). Administrative data are limited in the ability to identify parkinsonism. The ICD-9 CM code, 332.0, which is generally considered the code to identify Parkinson's disease, did not distinguish between parkinsonism and Parkinson's disease.
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PMID:Identifying and distinguishing cases of parkinsonism and Parkinson's disease using ICD-9 CM codes and pharmacy data. 1583 54

Males have a higher risk for developing Parkinson's disease and parkinsonism after ischemic stroke than females. Although estrogens have been shown to play a neuroprotective role in Parkinson's disease, there is little information on androgens' actions on dopamine neurons. In this study, we examined the effects of androgens under conditions of oxidative stress to determine whether androgens play a neuroprotective or neurotoxic role in dopamine neuronal function. Mitochondrial function, cell viability, intracellular calcium levels, and mitochondrial calcium influx were examined in response to androgens under both nonoxidative and oxidative stress conditions. Briefly, N27 dopaminergic cells were exposed to the oxidative stressor, hydrogen peroxide, and physiologically relevant levels of testosterone or dihydrotestosterone, applied either before or after oxidative stress exposure. Androgens, alone, increased mitochondrial function via a calcium-dependent mechanism. Androgen pretreatment protected cells from oxidative stress-induced cell death. However, treatment with androgens after the oxidative insult increased cell death, and these effects were, in part, mediated by calcium influx into the mitochondria. Interestingly, the negative effects of androgens were not blocked by either androgen or estrogen receptor antagonists. Instead, a putative membrane-associated androgen receptor was implicated. Overall, our results indicate that androgens are neuroprotective when oxidative stress levels are minimal, but when oxidative stress levels are elevated, androgens exacerbate oxidative stress damage.
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PMID:Oxidative stress defines the neuroprotective or neurotoxic properties of androgens in immortalized female rat dopaminergic neuronal cells. 2395 38

Sleep disturbances in Parkinson's disease and parkinsonism (such as atypical parkinsonian disorders like multiple system atrophy, progressive supranuclear palsy, dementia with Lewy bodies and corticobasal degeneration) are multifactorial and as such treatment needs to be tailored to the specific patient case and sleep dysfunction. One also has to consider drug-related effects on sleep architecture. This article provides an overview of the therapeutic options for nocturnal problems in Parkinson`s disease and atypical parkinsonian disorders.
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PMID:Therapeutic options for nocturnal problems in Parkinson's disease and atypical parkinsonian disorders. 2469 17

The coronavirus disease 2019 (COVID-19) pandemic has upended daily life and neurologic care for most patients, including those with Parkinson's disease and parkinsonism. Disruptions to routine care, high volumes of patient and caregiver calls, and our patients' risk of infection and complications inspired a proactive COVID-19 outreach program. This program targets patients with advanced Parkinson's disease and related disorders, specifically those who are homebound, receiving or eligible for palliative care, and/or lacking support networks. We describe the program and practical strategies providers can implement to support wellbeing and successful telehealth uptake during this time of social isolation and gradual reopening.
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PMID:Novel Outreach Program and Practical Strategies for Patients with Parkinsonism in the COVID-19 Pandemic. 3280 3