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 activity of DBH enzyme was measured in plasma of 7 non treated patients suffering from Parkinson's disease; a 10 mg dose of Bromocryptine was administered per os to these patients. Attained results were compared to the enzyme activity in a group of control of 7 healthy individuals. It was pointed out that in patients suffering from Parkinson's disease the decrease of DBH level in plasma after the administration of Bromocryptine was of 32.6% +/- SE 4.4% while in the group of control the decrease was only of 15% +/- SE 4.9%. This decrease in the plasmatic level of the enzyme after the administration of Bromocryptine should be due to the marked antagonistic activity of Bromocryptine on pre-synaptic dopaminergic receptors. This should mean that peripheric pre-synaptic dopaminergic receptors are involved in the physiopathology of Parkinson's disease.
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PMID:[Effect of bromocriptine on secretion of the enzyme dopamine-B-hydroxylase (DBH) in patients with Parkinson's disease]. 55 Feb 90

In a group of patients with Parkinson disease there was no difference in plasma DBH activity between cases treated with L-Dopa and not treated. These patients tend to have an elevated activity of erythrocyte AChE.
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PMID:Plasma dopamine-beta-hydroxylase and erythrocyte acetylcholinesterase in a group of patients with Parkinson disease. 65 Feb 7

Plasma dopamine-beta-hydroxylase was studied in 96 subjects, 33 of them controls and 63 of them patients (Parkinson's disease, chronic chorea, torsion dystonia, postural tremor and epilepsy). Only the epileptics showed a significant decrease in the average level of dopamine-beta-hydroxylase activity in comparison with the controls. During the cold test, DBH did not vary except in one case. On the other hand, during epileptic attacks, DBH activity underwent considerable fluctuations. Therefore, except in special pathological conditions, such as epileptic attacks, measurement of plasma or serum DBH activity is of limited value for neurological pathology and is not a good indication of the activity of the sympathetic nervous system.
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PMID:[Dopamine beta hydroxylase. Value and limits of its study in neurology]. 94 Sep 70

Patients with Parkinson's disease have received intracerebral transplants of autologous adrenal medulla in the attempt to counteract their severe motor dysfunctions. Unfortunately, in the majority of cases, clinical improvement has not persisted and there has been extremely poor survival of the grafts. Based on the recent observations of long-term viability of adrenal medulla grafts in the interior of transected peripheral nerves, adrenal medulla/peripheral nerve complexes were constructed in the brain to promote extended viability of chromaffin cells. A three-step, time-dependent transplantation procedure is described that results in a 100% survival rate of the adrenal medulla graft. The grafts consist of a stable population of approximately 2.0 x 10(3) chromaffin cells that survive for at least 6 months (longest time point studied): Immunoreactivity to catecholamine-related enzymes (tyrosine hydroxylase, dopamine beta-hydroxylase) and the low-affinity NGF receptor (192-IgG) are expressed by the chromaffin cells. The ultrastructural characteristics of the cells are normal and comparable to their in vivo counterparts. Construction of these peripheral nerve/adrenal medulla complexes evidently improves local conditions in and around the grafts, enabling the chromaffin cells to remain viable. This new methodology achieves the goal of reliable and extended survival of the adrenal medulla graft after intracerebral transplantation. The enhanced longevity now provides an opportunity to reevaluate the efficacy of the adrenal medulla transplant to ameliorate the functional disorders associated with striatal dopamine depletion, especially over long time periods.
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PMID:Peripheral nerve segments promote consistent long-term survival of adrenal medulla transplants in the brain. 136 82

Intracerebral adrenal medulla grafts have been used in human patients as an experimental treatment for Parkinson's disease, based on studies in animal models of this disorder. However, alterations in chromaffin cell properties after transplantation and the factors controlling graft survival are poorly understood. Since cell adhesion molecules (CAMs) are involved in regeneration and development of neural tissue in vivo and in vitro, the present study was undertaken to determine the expression of CAMs in adrenal medulla isografts. Fragments of rat adrenal medulla were implanted into the right lateral ventricle. The majority of grafts survived quite well, for up to 2 months (the longest studied period). The implanted chromaffin cells did not develop extensive processes. The cells retained tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) immunoreactivity, while phenylethanolamine N-methyltransferase (PNMT) expression was decreased. Surviving transplanted chromaffin cells showed enhancement and spreading of surface L1/Ng-CAM expression as compared to normal chromaffin cells in adrenal medulla. The implanted chromaffin cells demonstrated only partial conversion to neuronal phenotypes. These chromaffin cells did not develop extensive processes, but showed an enhancement of L1/Ng-CAM expression. Surviving chromaffin cells were accompanied by reorganization of their closely associated extracellular matrix (ECM). As compared to normal in situ adrenal medulla, graft ECM demonstrated a substantial increase of L1/Ng-CAM and laminin immunoreactivities and a distinct decrease in J1/tenascin expression. Some adrenal medulla grafts degenerated, particularly when misplaced within the host brain parenchyma. In these cases the grafts showed fragmentation of ECM and gradual disappearance of CAMs. These results suggest that surviving adrenal medulla grafts exhibit increased synthesis of certain CAMs by chromaffin cells, which may be involved in interactions between chromaffin cells and the surrounding ECM. It is speculated that both surviving and degenerating adrenal medulla grafts could provide CAMs and ECM components including laminin to host brain and this way contribute to functional effects of grafts.
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PMID:Cell adhesion molecules in adrenal medulla grafts: enhancement of chromaffin cell L1/Ng-CAM expression and reorganization of extracellular matrix following transplantation. 220 83

A sandwich enzyme immunoassay (EIA) was established by using purified beta 2-microglobulin (beta 2-MG) as a standard protein and a polyclonal antibody raised against human beta 2-MG. The EIA was applied for the measurement of beta 2-MG levels in human cerebrospinal fluid (CSF) from parkinsonian patients and control patients devoid of neurological diseases. beta 2-MG contents in CSF of the control group and the parkinsonian group were 1.81 +/- 0.11 micrograms/ml CSF and 0.63 +/- 0.09 microgram/ml CSF, respectively. Thus, beta 2-MG content in CSF was reduced in parkinsonian patients to less than 35% of the control value (P less than 0.005). We had previously reported that the activity and content of dopamine beta-hydroxylase (DBH) were decreased in CSF from parkinsonian patients. A significant positive correlation (r = 0.87) was observed between the beta 2-MG content and DBH activity for CSF from 45 patients. These results suggest a probable link between an immunological change and the changes in catecholaminergic neurons in Parkinson's disease.
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PMID:Beta 2-microglobulin decrease in cerebrospinal fluid from parkinsonian patients. 268 94

The concentration of neuropeptide Y has been determined in the cortex and hippocampus of subjects with Parkinson's disease and compared to changes of activity of dopamine beta-hydroxylase and concentration of somatostatin. Despite a marked reduction in the concentration of somatostatin in the severely demented subject, in both cortex and hippocampus, no significant change in concentration of NPY was found in either region. This finding therefore suggests that the majority of NPY within the cortex is independent of somatostatin. This study provides some further evidence of neurochemical similarities between the dementia of Parkinson's disease and Alzheimer's disease.
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PMID:Dissociation of neuropeptide Y and somatostatin in Parkinson's disease. 286 Sep 55

Recent reports of adrenal medullary autografts in patients with Parkinson's disease raise several important questions with respect to the cell types actually being transplanted as well as the potential for chromaffin cell banking prior to neural transplantation. In this study, we determined the general morphological characteristics of the human adrenal medulla and assessed factors important for the maintenance of cultured chromaffin cells for later use as transplants. The human adrenal medulla contained islands of cortical cells scattered throughout the gland as well as Schwann cells, nerve endings, endothelial cells, pericytes, isolated ganglionic neurons, and connective tissue elements such as fibroblasts and smooth muscle cells. Because many of these cell types are mitotically active, transplantation of medullary fragments that contain these cells could have far-reaching consequences. One approach that could circumvent the problems arising from multiple cell types in the medulla is differential plating of chromaffin cells prior to transplantation. Differential plating yielded relatively pure populations of chromaffin cells that demonstrated excellent viability if processed within 2 hours after cessation of the gland's circulation. Chromaffin cells cultured in the presence of nerve growth factor exhibited a neuronal phenotype, possessed catecholamine histofluorescence, and displayed tyrosine hydroxylase- and dopamine beta-hydroxylase-like immunoreactivity. The sex and age of the donor did not affect cell viability or morphological characteristics.
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PMID:Organization, fine structure, and viability of the human adrenal medulla: considerations for neural transplantation. 320 12

In parkinsonian brain, TH and the BP cofactor, as well as DBH and PNMT with phenylethanolamine as substrate, are decreased. However, decrease in AADC with L-DOPA as substrate was not statistically significant. TH activity has also been shown to be decreased in striatonigral degeneration and Shy-Drager syndrome. TH reduction only in striatum but not in substantia nigra was found in a case of juvenile Parkinson's disease. Changes in AADC with L-DOPA or L-5-HTP as substrates varied in parkinsonian brains. PNMT with norepinephrine as substrate was also significantly decreased in parkinsonian brains. After administration of tyrosine to mice, the BP concentration was increased in striatum, adrenals, and serum. Mean BP concentration in serum of parkinsonian patients was slightly but significantly lower than that in controls. The serum BP increased three- to sevenfold in response to an oral tyrosine load in controls, whereas there was no increase or only a minor one (less than threefold) in parkinsonian patients. Our present results indicate that all catecholamine-synthesizing enzymes and BP synthesis may be impaired in Parkinson's disease.
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PMID:Catecholamine-related enzymes and the biopterin cofactor in Parkinson's disease and related extrapyramidal diseases. 614 12

1. Dopamine beta-hydroxylase is stored and released with catecholamines by exocytosis from secretory vesicles in noradrenergic neurons and chromaffin cells. Although dopamine beta-hydroxylase enzymic activity is measurable in cerebrospinal fluid, such activity is unstable, and its relationship to central noradrenergic neuronal activity in humans is not clearly established. To explore the significance of cerebrospinal fluid dopamine beta-hydroxylase, we applied a homologous human dopamine beta-hydroxylase radioimmunoassay to cerebrospinal fluid, in order to characterize the properties and stability of cerebrospinal fluid dopamine beta-hydroxylase, as well as its relationship to central noradrenergic neuronal activity and its variation in disease states such as hypertension, renal failure, Parkinsonism and congenital dopamine beta-hydroxylase deficiency. 2. Authentic, physically stable dopamine beta-hydroxylase immunoreactivity was present in normal human cerebrospinal fluid at a concentration of 31.3 +/- 1.4 ng/ml (range: 18.5-52.5 ng/ml), but at a 283 +/- 27-fold lower concentration than that found in plasma. Cerebrospinal fluid and plasma dopamine beta-hydroxylase concentrations were correlated (r = 0.67, P = 0.001). Some degree of local central nervous system control of cerebrospinal fluid dopamine beta-hydroxylase was suggested by incomplete correlation with plasma dopamine beta-hydroxylase (with an especially marked dissociation in renal disease) as well as the lack of a ventricular/lumbar cerebrospinal dopamine beta-hydroxylase concentration gradient. 3. Cerebrospinal fluid dopamine beta-hydroxylase was not changed by the central alpha 2-agonist clonidine at a dose that diminished cerebrospinal fluid noradrenaline, nor did cerebrospinal fluid dopamine beta-hydroxylase correspond between subjects to cerebrospinal fluid concentrations of noradrenaline or methoxyhydroxyphenylglycol; thus, cerebrospinal fluid dopamine beta-hydroxylase concentration was not closely linked either pharmacologically or biochemically to central noradrenergic neuronal activity. 4. Cerebrospinal fluid dopamine beta-hydroxylase was not changed in essential hypertension. In Parkinson's disease, cerebrospinal fluid dopamine beta-hydroxylase was markedly diminished (16.3 +/- 2.9 versus 31.3 +/- 1.4 ng/ml, P < 0.001) and rose by 58 +/- 21% (P = 0.02) after adrenal-to-caudate chromaffin cell autografts. In congenital dopamine beta-hydroxylase deficiency, lack of detectable dopamine beta-hydroxylase immunoreactivity in cerebrospinal fluid or plasma suggests absent enzyme (rather than a catalytically defective enzyme) as the origin of the disorder. 5. We conclude that cerebrospinal fluid dopamine beta-hydroxylase immunoreactivity, while not closely linked to central noradrenergic neuronal activity, is at least in part derived from the central nervous system, and that its measurement may be useful in both the diagnosis and treatment of neurological disease.
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PMID:Dopamine beta-hydroxylase immunoreactivity in human cerebrospinal fluid: properties, relationship to central noradrenergic neuronal activity and variation in Parkinson's disease and congenital dopamine beta-hydroxylase deficiency. 814 25


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