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)

Dopamine D3 receptor was studied in peripheral mononuclear cells of high-normal, stage 1, stage 2, and stage 3 essential hypertensives using a radioligand binding assay technique with [3H]-7-hydroxy-N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT) as a radioligand. A group of de novo Parkinsonian patients was also examined as a reference group of impaired dopaminergic function. [3H]-7-OH-DPAT was bound specifically to human peripheral mononuclear cells in a manner consistent with the labeling of a dopamine D3 receptor. No changes in free dopamine, norepinephrine, epinephrine and aldosterone levels, renin activity, dissociation constant of [3H]-7-OH-DPAT binding, or the pharmacological profile of [3H]-7-OH-DPAT binding were found between normotensive control subjects and essential hypertensives or Parkinsonians. The density of peripheral mononuclear cell [3H]-7-OH-DPAT binding sites increased in essential hypertensives parallel to blood pressure value augmentation. A higher density of [3H]-7-OH-DPAT binding sites was found in Parkinsonians. In these patients, the density of [3H]-7-OH-DPAT binding sites was similar to that observed in high-normal subjects and in stage 1 essential hypertensives. The increased density of peripheral mononuclear cell dopamine D3 receptor in hypertension as well as in Parkinson's disease may represent an upregulation mechanism consequent to impaired dopaminergic function. In view of the difficulty in identifying markers of peripheral dopamine function, analysis of dopamine D3 receptor in peripheral mononuclear cells may help evaluate whether the dopaminergic system is involved in hypertension.
Hypertension 1997 Dec
PMID:Dopamine D3 receptor in peripheral mononuclear cells of essential hypertensives. 940 84

A wide variety of anatomic and histological alterations are common in brains of aged individuals. However, identification of intrinsic aging changes--as distinct from changes resulting from cumulative environmental insult--is problematic. Some degree of neuronal and volume loss would appear to be inevitable, but recent studies have suggested that the magnitudes of such changes are much less than previously thought, and studies of dendritic complexity in cognitively intact individuals suggest continuing neuronal plasticity into the eighth decade. A number of vascular changes become more frequent with age, many attributable to systemic conditions such as hypertension and atherosclerosis. Age-associated vascular changes not clearly linked to such conditions include hyaline arteriosclerotic changes with formation of arterial tortuosities in small intracranial vessels and the radiographic changes in deep cerebral white matter known as "leukoaraiosis." Aging is accompanied by increases in glial cell activation, in oxidative damage to proteins and lipids, in irreversible protein glycation, and in damage to DNA, and such changes may underlie in part the age-associated increasing incidence of "degenerative" conditions such as Alzheimer disease and Parkinson disease. A small number of histological changes appear to be universal in aged human brains. These include increasing numbers of corpora amylacea within astrocytic processes near blood-brain or cerebrospinal fluid-brain interfaces, accumulation of the "aging" pigment lipofuscin in all brain regions, and appearance of Alzheimer-type neurofibrillary tangles (but not necessarily amyloid plaques) in mesial temporal structures.
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PMID:Aging-associated changes in human brain. 941 75

The aetiology of the common dementias of old age remains incompletely understood. Here we describe some of the biological, neurophysiological and psychological changes associated with ageing of the human brain, in terms of those that occur throughout life and those that are characteristic of senescence. Age-dependent diseases, such as Alzheimer's disease (AD), idiopathic Parkinson's disease (IPD) and dementia with Lewy bodies (DLB), are considered from these viewpoints, and risk factors described. Vascular dementia (VaD) is related to hypertension and atherosclerosis and detailed description of its pathogenesis is outside the scope of this review. The importance of age as the main risk factor raises basic questions about the relationship of these diseases to the ageing process itself. Similarities and differences between ageing and disease may be important for a rational approach to prevention and treatment of cognitive decline and dementia in later life.
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PMID:Some developments in brain ageing and dementia. 949 98

Many efforts have been made to trace the causes of Alzheimer's disease (AD). There are, however, many points of controversy among reports from the same country as well as among reports from different countries. The current study is a case-control study to determine the risk factors in the development of AD in Greece. Sixty-five patients with AD and 69 age-matched controls were examined. All patients with AD fulfilled the DSM-IV criteria for AD and NINCDS-ADRDA criteria for probable AD. Demographic characteristics such as gender, current marital status, who he/she is living with, education, main place of residence in childhood, adulthood, and late life, occupational hazards, patient's medical history (history of diabetes mellitus and hypertension), life habits like alcohol consumption and smoking, and a history of head trauma, heart attack, stroke, parkinsonism, or depression were collected from the subject or from an informant. A family history of selected diseases (hypertension, diabetes mellitus, dementia, Parkinson's disease, Down's syndrome, stroke) was also elicited. Ages of father and mother at birth were also recorded. Chi-square test, Kruskal-Wallis analysis of variance, cluster analysis, and logistic regression analysis were used for statistical analysis. The results (chi-square test) showed a statistically significant difference between patients with dementia of the Alzheimer type and controls as far as marital status (p = .04), the subject's history of major depressive episode (p = .02), and family history of dementia (p = .002) were concerned. Logistic regression analysis results produced a complex model of family aggregation of dementia, with patients with a history of depression and family history of dementia having an up to seven times higher risk of developing AD. These findings, especially a family history of dementia, are consistent with most of the literature.
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PMID:Risk factors for clinically diagnosed Alzheimer's disease: a case-control study of a Greek population. 951 31

For patients with Parkinson's disease who have become unresponsive to pharmacotherapy or have developed severe motor complications due to medical therapy, a number of symptomatic neurosurgical interventions are available: thalamotomy, thalamic stimulation and pallidotomy. These stereotactic operations are performed under local anaesthesia. The target is located using anatomical and physiological techniques, after which the neuro-ablative or neuromodulatory procedure is performed. The choice of the target depends on the symptoms of the patient that most impair daily functioning. In case of dominating tremor, thalamic surgery is performed. Patients who are mainly incapacitated by rigidity, hypokinesia or pharmacotherapy-induced dyskinesias are suitable candidates for pallidotomy. Contraindications are cognitive dysfunction, severe disturbance of gait and balance, advanced cerebral atrophy on CT or MRI, limited life expectancy and a poor general condition enhancing surgical risk, e.g. coagulation disorders or uncontrolled hypertension. Surgical treatment of Parkinson's disease is being carried out in clinical trials in the Netherlands in the Academic Medical Centre in Amsterdam, the Academic Hospital in Groningen and the St. Elisabeth Hospital in Tilburg.
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PMID:[Neurosurgical stereotactic treatment in Parkinson's disease]. 955 82

Physical disorders and pharmacotherapy for all 134 people with mental retardation ages 65 years and over living in Leicestershire, United Kingdom, were examined. Results were compared with a randomly selected group of 73 younger adults with mental retardation. Group comparisons revealed higher rates of urinary incontinence, immobility, hearing impairments, arthritis, hypertension, and cerebrovascular disease among the older group. The younger group had higher rates of dermatological disorders; congenital heart disease; ear, nose, and throat (ENT) disorders; and neurological disorders (excluding Parkinson disease). The older group took more drugs for physical illness. The effect of ageing on physical morbidity outweighs the effect of people with more severe mental retardation dying younger: Older people with mental retardation have significant physical health needs.
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PMID:Clinical study of the effects of age on the physical health of adults with mental retardation. 960 67

Age-related white matter injury has been recognized increasingly with the improvement of brain imaging technology. Arteriosclerosis and venous collagenosis, which occur with aging, result in a spectrum of white matter changes that range from periventricular to subcortical and deep white matter hyperintensities best seen on T2 weighted magnetic resonance imaging. These white matter changes are associated not only with aging, but with hypertension and silent infarctions. Loss of brain volume and accumulation of iron in putamen occur with normal, healthy aging. This article discusses the imaging appearance of healthy aging and pathological correlates of similar appearing alterations. The imaging findings of the most common neurodegenerative disorders, Alzheimer's and Parkinson's disease, are highlighted.
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PMID:Neuroimaging of the aging brain. 966 38

Selegiline (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B (MAO-B) is widely used in the treatment of Parkinson's disease. As the first MAO-B inhibitor approved for the treatment of Parkinson's disease, concerns were raised about the safety of the drug based on the adverse effect profiles of older, nonselective MAO inhibitors. Unlike the nonselective MAO inhibitors, selegiline does not significantly potentiate tyramine-induced hypertension (the 'cheese effect') at the dosages (5 to 10 mg daily) used for the treatment of Parkinson's disease. Selegiline has been well tolerated when given alone. The most frequent adverse events seen during monotherapy have been insomnia, nausea, benign cardiac arrhythmias, dizziness and headache. When combined with levodopa, selegiline can potentiate the typical adverse effects of levodopa, if the dose of levodopa is not reduced sufficiently. Thus, the most common adverse effects associated with this combination are nausea, dizziness, fatigue, constipation and insomnia. At the later stages of Parkinson's disease when fluctuations in disability occur, peak dose dyskinesias, psychiatric complications like hallucinations and insomnia, and orthostatic hypotension are further potentiated by selegiline. Mortality was recently reported to be increased when selegiline and levodopa were given together in comparison with treatment with levodopa alone, but a large meta-analysis of 5 long term studies and 4 separate studies did not support this conclusion. Selegiline seems to be generally well tolerated in combination with other drugs. However, when pethidine (meperidine) has been given to patients who are receiving selegiline therapy, severe adverse effects have been reported. Thus, the concomitant use of these drugs is not recommended. A low tyramine diet is recommended if selegiline is used together with nonselective MAO inhibitors or the selective, reversible MAO-A inhibitor, moclobemide. Several adverse effects have been reported when fluoxetine and selegiline have been used together. A recent survey revealed that the incidence of a true serotonin syndrome is, however, very low with this combination. Concomitant use of selegiline and other selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs) like citalopram, which have generally less interactions than fluoxetine, seems to be well tolerated. Nevertheless, caution is advised when combining a SSRI or a tricyclic antidepressant and selegiline.
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PMID:Safety of selegiline (deprenyl) in the treatment of Parkinson's disease. 967 55

A questionnaire-based case-control study was carried out on 86 patients with neurologist-confirmed idiopathic Parkinson's disease (PD) and 86 controls similar in sex and age. The control group was recruited in outpatient specialist centers of the same University Hospital (glaucoma, psoriasis vulgaris, essential arterial hypertension and renal diseases). Exposure was defined as occupational or residential contact with a given factor for at least 10 consecutive years prior to the onset of PD. Smoking habits were defined by exclusion of those subjects who never smoked. The following risk factors were identified: cranial trauma (OR: 2.88; 95% CI: 0.98-8.49), well water use (OR: 2.78; 95% CI: 1.46-5.28) and occupational exposure to industrial chemicals (OR: 2.13; 95% CI: 1.16-3.91). Among industrial chemicals, only organic solvents were identified as significant risk factors for PD (O.R. : 2.78, 95% C.I. : 1.23-6.26). Whereas no exposure to neurotoxic metals occurred among controls, making the assessment of the O.R. impossible, exposure pesticides and herbicides was similar in the two groups (O.R. : 1.15; 95% C. : 0.56-2-36). Smoking habits was negatively associated with PD (OR: 0.41; 95% CI: 0.22-0.75), confirming the "protective" role of tobacco smoking suggested by many studies. As a whole, these results support the role of environmental factors in the etiology of PD.
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PMID:A case-control study of occupational and environmental risk factors for Parkinson's disease in the Emilia-Romagna region of Italy. 974 32

A prevalence study of Parkinson's disease (PD) was conducted in the rural town of Nambour, Australia. There were 5 cases of PD in a study population of 1207, yielding a crude prevalence ratio of 414 per 100,000 (95% confidence interval; 53-775). We performed a separate case-control study involving 224 patients with PD and 310 controls from South East Queensland and Central West New South Wales, to determine which factors increase the risk for PD in Australia. A positive family history of PD was the strongest risk factor for the development of the disease (odds ratio = 3.4; p < 0.001). In addition, rural residency was a significant risk factor for PD (odds ratio = 1.8, p < 0.001). Hypertension, stroke and well water ingestion were inversely correlated with the development of PD. There was no significant difference between patients and controls for exposure to herbicides and pesticides, head injury, smoking or depression. The high prevalence of PD in Nambour may be explained by rural residency. However, the most significant risk factor for PD was a positive family hisotry. This demonstrates the need for improved understanding of the genetic nature of the disease.
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PMID:The epidemiology of Parkinson's disease in an Australian population. 977 97


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