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)

While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio = 2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio = 0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Neurol 1991 Sep
PMID:The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. 195 12

The influence of age of onset of Parkinson's disease on the severity and the pattern of motor symptoms was investigated by comparing the motor scores with and without levodopa therapy in two groups of patients divided according to age of onset (early less than 50, late greater than 60 years) and matched for disease duration (n = 69 in each group, Study I). The baseline score, that is, the motor disability of patients when off levodopa, was similar in the early- and late- onset groups. In contrast, the residual motor score, assessed when the effect of levodopa treatment was maximum and stable, was significantly higher in the late onset group. When the two groups of patients were matched, in addition, for their residual motor score, (n = 54 in each group, Study II), no difference was observed between the early and late onset groups, except for gait disorder which was more severe in older patients. These results suggest that age of onset mainly affects the response to levodopa therapy, because it may increase the prevalence of non-dopaminergic lesions of the brain, including those responsible for gait disorders.
J Neurol Neurosurg Psychiatry 1991 Sep
PMID:Does ageing aggravate parkinsonian disability? 195 94

Cognitive and cerebral blood flow (CBF) lateral asymmetries have been quantified in 23 right handed patients with lateralised idiopathic Parkinson's disease. Thirteen patients who had predominant right-sided symptoms (RPD) were compared with ten who had predominant left-sided symptoms (LPD). The patient subgroups were matched for age, education, duration of illness, disease severity and medication. Normalised asymmetries scores were calculated from the data obtained with a test battery and SPECT. No correlation was found between laterality of motor Parkinsonian symptoms and cognitive or haemodynamic asymmetry scores.
J Neurol Neurosurg Psychiatry 1991 Sep
PMID:Cognition and cerebral blood flow in lateralised parkinsonism: lack of functional lateral asymmetries. 195 95

Regional cerebral perfusion was evaluated by single photon emission tomography (SPECT) using (99mTc)-HM-PAO as a tracer, in thirty Parkinsonian patients with (n = 15) or without (n = 15) dementia, nineteen patients with dementia of the Alzheimer type (DAT) and thirteen control subjects. HM-PAO uptake was measured in the frontal, parietal, temporal and occipital cortex and tracer perfusion was expressed as cortical/cerebellar activity ratios. Regional HM-PAO ratios in nondemented Parkinsonian patients did not differ from controls, whereas in demented patients with Parkinson's disease (DPD) a significant reduction was found in the parietal, temporal and occipital cortex. Tracer uptake ratios were significantly reduced in all regions in the DAT group. Thus DPD and DAT shared a common pattern of marked posterior hypoperfusion, although the perfusion defect was greater and more extensive in the DAT patients.
J Neurol Neurosurg Psychiatry 1991 Sep
PMID:(99mTc)-HM-PAO SPECT and cognitive impairment in Parkinson's disease: a comparison with dementia of the Alzheimer type. 143 75

Receptors for dopamine have been classified into two functional types, D1 and D2. They belong to the family of receptors acting through G (or guanine nucleotide-binding) proteins. D2 receptors inhibit adenylyl cyclase, but D1 receptors stimulate adenylyl cyclase and activate cyclic AMP-dependent protein kinases. Dopamine D1 and D2 receptors are targets of drug therapy in many psychomotor disorders, including Parkinson's disease and schizophrenia, and may also have a role in drug addiction and alcoholism. D1 receptors regulate neuron growth and differentiation, influence behaviour and modify dopamine D2 receptor-mediated events. We report here the cloning of the D1 receptor gene, which resides on an intronless region on the long arm of chromosome 5, near two other members of the G-linked receptor family. The expressed protein, encoded by 446 amino acids, binds drugs with affinities identical to the native human D1 receptor. The presence of a D1 receptor gene restriction fragment length polymorphism will be helpful for future disease linkage studies.
Nature 1990 Sep 06
PMID:Human dopamine D1 receptor encoded by an intronless gene on chromosome 5. 197 40

A dopamine receptor has been characterized which differs in its pharmacology and signalling system from the D1 or D2 receptor and represents both an autoreceptor and a postsynaptic receptor. The D3 receptor is localized to limbic areas of the brain, which are associated with cognitive, emotional and endocrine functions. It seems to mediate some of the effects of antipsychotic drugs and drugs used against Parkinson's disease, that were previously thought to interact only with D2 receptors.
Nature 1990 Sep 13
PMID:Molecular cloning and characterization of a novel dopamine receptor (D3) as a target for neuroleptics. 197 44

Somatostatin may play a role in several neurodegenerative diseases. Somatostatin concentrations are depleted in cerebral cortex in both Alzheimer's disease and in the dementia that accompanies Parkinson's disease. Somatostatin neurons in both illnesses are markedly dystrophic and may be reduced in number. In Huntington's disease, somatostatin concentrations are increased in the basal ganglia, as is the density of somatostatin neurons. The precise role of somatostatin changes in the pathophysiology of these illnesses requires further study.
Metabolism 1990 Sep
PMID:Somatostatin in neurodegenerative illnesses. 197 4

Several studies have reported an apparent protective effect of cigarette smoking for the risk of idiopathic Parkinson's disease (IPD). These observations are supported by neurochemical studies demonstrating enhancement of central dopaminergic neurotransmission by nicotine. We studied the prevalence and severity of neuroleptic-induced parkinsonism (NIP) in relation to cigarette smoking in a homogeneous sample of 130 psychiatric inpatients receiving long-term neuroleptic treatment. Despite the fact that smokers had significantly higher dosage of neuroleptics during the month prior to evaluation and longer exposure to medication, they presented with significantly less prevalence and severity of NIP than nonsmokers. These findings suggest that the inverse association between smoking and IPD may apply to NIP.
Biol Psychiatry 1990 Sep 15
PMID:Cigarette smoking and neuroleptic-induced parkinsonism. 197 78

The diverse physiological actions of dopamine are mediated by its interaction with two basic types of G protein-coupled receptor, D1 and D2, which stimulate and inhibit, respectively, the enzyme adenylyl cyclase. Alterations in the number or activity of these receptors may be a contributory factor in diseases such as Parkinson's disease and schizophrenia. Here we describe the isolation and characterization of the gene encoding a human D1 dopamine receptor. The coding region of this gene is intronless, unlike the gene encoding the D2 dopamine receptor. The D1 receptor gene encodes a protein of 446 amino acids having a predicted relative molecular mass of 49,300 and a transmembrane topology similar to that of other G protein-coupled receptors. Transient or stable expression of the cloned gene in host cells established specific ligand binding and functional activity characteristic of a D1 dopamine receptor coupled to stimulation of adenylyl cyclase. Northern blot analysis and in situ hybridization revealed that the messenger RNA for this receptor is most abundant in caudate, nucleus accumbens and olfactory tubercle, with little or no mRNA detectable in substantia nigra, liver, kidney, or heart. Several observations from this work in conjunction with results from other studies are consistent with the idea that other D1 dopamine receptor subtypes may exist.
Nature 1990 Sep 06
PMID:Molecular cloning and expression of the gene for a human D1 dopamine receptor. 214 34

We measured the binding of the vesicular acetylcholine transport blocker [3H]vesamicol (2-[4-phenylpiperidino] cyclohexanol; AH-5183) to autopsied frontal cortex and amygdala of patients from 4 disorders having a marked brain cholinergic reduction, namely Alzheimer's disease, Parkinson's disease with dementia, dominantly inherited olivopontocerebellar atrophy and Down's syndrome. Although mean activity of the specific cholinergic marker enzyme choline acetyltransferase (ChAT) was markedly reduced by about 60% in frontal cortex in the 4 patient groups and by 80% or greater in amygdala of the Alzheimer's and Down's syndrome patients, [3H]vesamicol binding density was, on average, either normal or only slightly reduced as compared with the controls. This discrepancy suggests that in human brain [3H]vesamicol binding is either not preferentially localized to cholinergic nerve endings or, in these cholinergic deficiency syndromes, a substantial proportion of the vesamicol binding sites persist on cholinergic nerve terminals despite loss of ChAT activity.
Neurosci Lett 1990 Sep 18
PMID:[3H]vesamicol binding in human brain cholinergic deficiency disorders. 215 Dec 94


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