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)

Post-mortem brain material from control and Parkinson's disease patients was examined to elucidate further the neurochemistry of this disease and to determine the mechanism of action of L-dopa as a therapeutic agent. The activities of L-aromatic amino acid decarboxylase (dopa D), tyrosine hydroxylase, monoamine oxidase and catechol-O-methyl transferase were examined; in addition the tissue levels of dopa, 3-O-methyldopa, dopamine (DA) and homovanillic acid (HVA) were determined. In the non-dopa-treated Parkinsonian patients, the greatest decreases were detected for striatal DA and dopa D, with homovanillic acid and tyrosine hydroxylase levels showing a lesser change. The activities of monoamine oxidase and catechol-O-methyl transferase in the striatal nuclei were not different from the controls. The putamen was consistently the most severely affected region. Dopa and 3-O-methyldopa were detectable in all brain areas only in those patients treated with L-dopa shortly before death. The mean concentrations of DA in the striatum of these patients were 1) 9 to 15 times higher than those in non-dopa-treated patients, 2) related to the time before death of the last dose of L-dopa and 3) greater in the striatum of patients clinically classified as "good responders" as compared to "poor responders." Although L-dopa therapy increased homovanillic acid levels in all brain areas, a preferential increase was observed in the striatum. It was concluded that L-dopa's principal therapeutic effects in Parkinson's disease are consistent with its transformation to DA in the striatum.
J Pharmacol Exp Ther 1975 Dec
PMID:The neurochemistry of Parkinson's disease: effect of L-dopa therapy. 0 Apr 89

On the basis of reports in the literature and of our own clinical experience it appears that melanocyte inhibiting factor (MIF) is a very promising therapeutic agent in the management of Parkinson's disease. Besides theoretical considerations relating to biochemical and pathophysiological spheres, the question of the current dosage for clinical usage seems to be of the utmost importance. We are of the opinion that the currently-employed dosage of 400 mg daily is still too low. Hence, the present investigation will be continued with a view to establishing the optimum dosage for maximal therapeutic effect.
Wien Klin Wochenschr 1975 Dec 26
PMID:[Infusion therapy with mif (melanocyte inhibiting factor) in Parkinson's disease (author's transl)]. 0 15

The metabolic pathways for five transmitters in the basal ganglia are briefly described; the results of determinations of their concentrations, of their rate-limiting enzymes and of their degradation products are summarized. The changes found in Parkinson's disease are described. While dopamine synthesis in the basal ganglia is defective in this condition, abnormalities of other transmitters occur, and their possible significance is discussed.
Postgrad Med J 1977 Dec
PMID:The biochemistry of the basal ganglia and Parkinson's disease. 2 9

It is known that a single dose of a neuroleptic can elicit dopaminergic supersensitivity in animals. On the other hand, the clinical syndrome of tardive dyskinesia takes many months of years to develop. To resolve this apparent discrepancy, it is possible that subclinical or latent tardive dyskinesia is fully compensated in most patients taking neuroleptics. In others, where the tardive dyskinesia is full-blown and grossly apparent, the dopaminergic supersensitivity may be decompensated. Such compensatory and decompensatory phases have been proposed earlier by Hornykiewicz (1974), in the case of Parkinson's Disease. Dopaminergic supersensitivity persists for a period proportional to the lenght of the neuroleptic treatment. It is not yet clear whether the relation between the length of treatment and the persistence of supersensitivity holds for very long treatments, but in principle the relationship might account for the persistence of tardive dyskinesia after years of neuroleptic pretreatment.
Psychopharmacology (Berl) 1978 Dec 15
PMID:Dopaminergic supersensitivity after neuroleptics: time-course and specificity. 3 74

A combination of levodopa and the extracerebrally acting decarboxylase inhibitor benserazide (ratio 4:1) (Madopar), was compared with levodopa alone in a controlled double-blind clinical multicenter trial on 94 patients with Parkinson's disease. During 4 months of therapy levodopa + benserazide proved superior to levodopa on several accounts. Nausea and vomiting occurred with statistically significant less severity and frequency. Clinical improvement expressed through improvement in Webster rating occurred sooner and was all together greater. The treatment schedules did not differ with regard to other side effects, in particular involuntary movements and reduction in supine blood pressure. Neither treatment seemed to influence liver function, renal function and hematological parameters.
J Neurol 1975 Dec 02
PMID:Levodopa alone and in combination with a peripheral decarboxylase inhibitor benserazide (Madopar) in the treatment of Parkinson's disease: A controlled clinical trial. 5 27

The CSF proteins have previously been very little investigated in the cerebellar syndrome of chronic alcoholism and in essential tremor. Such studies have been carried out more thoroughly by electrophoretic methods in Parkinson's disease but generally with normal results. In the present investigation the CSF proteins were examined by isoelectric focusing and quantitative paper electrophoresis in 10 patients with the cerebellar syndrome of chronic alcoholsm, 12 patients with Parkinson's disease and 16 subjects with essential tremor. Abnormal CSF proteins of very similar appearance were found on isoelectric focusing in the acidic pH interval 5.6-5.8 in 80% of the patients with the cerebellar syndrome of chronic alcoholism. In Parkinson's disease the most common aberration was evidence of nonspecific blood-CSF-barrier damage which occurred in half of the patients. In only 17% of these cases did other alterations appear, situated in the pH range alkaline to pH 5.8. Abnormal CSF proteins were found in 94% of the patients with essential tremor. The aberrant proteins appeared in both the acidic and alkaline pH regions, most frequently with anisoelectric point at pH 5.9, 7.2 and 9.3. There was a considerably higher frequency of CSF protein abnormalities in different pH ranges in patients with tremor of more pronounced degree as compared to those with only mild symptoms. The electrophoretic examinations failed to show any conclusive alterations. Barrier-damage patterns of mild or moderate degree or slightly increased levels of CSF beta1-globulin were occasionally found in all 3 diseases. The results indicate that isoelectric focusing of the CSF proteins may be of diagnostic value in the cerebellar syndrome of chronic alcoholism and in essential tremor but does not reveal any characteristic abnormalities in Parkinson's disease.
J Neurol Sci 1976 Dec
PMID:Isoelectric focusing and electrophoresis of the CSF proteins in tremor of different origins. 6 43

Computed tomographic examinations of parkinsonian patients revealed a high incidence of cerebral atrophy, in most cases a combination of cortical atrophy and ventricular enlargement. The present study considered the relationship between cerebral atrophy and physical signs indicating or promoting arteriosclerosis such as overweight, electrocardiographic changes, hypertension, calcification of the internal carotid artery and aorta as well as elongation of the aorta. The study is based on 173 treated and untreated parkinsonian patients (89 men, 84 women) aged from 37--84 years (mean 64.6), on whom CT was performed about 5.4 years after the onset of the first symptoms of the illness. The results demonstrate an increase of pathological CT findings as well as of calcification in the carotid siphon with advanced age. No correlation was found between the other items and increasing age. Further analysis of the relationship between cerebral atrophy and signs of arteriosclerosis revealed only a statistically relevant correlation with calcification of the carotid siphon, especially with calcification of the media. Since pathological CT findings and calcification of the internal carotid artery are both related to advanced age, whereas all the other items which may be considered to be indications of arteriosclerosis do not have any clear relationship, it is concluded that the cerebral atrophy in Parkinson's disease is not caused by arteriosclerosis.
J Neurol 1977 Dec 01
PMID:Relationship between arteriosclerosis and cerebral atrophy in Parkinson's disease. 7 48

The activities of the aminotransferases, GOT and GPT, were determined in the serum and cerebrospinal fluid of patients with Parkinson's disease, Huntington's chorea, Wilson's disease, amyotrophic lateral sclerosis (ALS), Friedreich's ataxia, phenylketonuria, and head injuries. 1. In patients with Huntington's chorea the activity of SGOT was lower than in controls (P = 0.02); in Friedreich's ataxia LGPT activity was decreased (P less than 0.001); in patients suffering from ALS SGOT (P = 0.005), SGPT (P less than 0.001) and LGOT (P less than 0.001) activities were increased. 2. Long-term treatment of Parkinson's disease and Wilson's disease with L-dopa resulted in an increase in SGOT, LGOT, and SGPT activity over approximately 2 months, with subsequent normalization of these enzyme activities in spite of continued therapy. Guanidine treatment led to an increase in aminotransferase activities in patients with ALS. Penicillamine caused a decrease in SGOT and SGPT activities in Wilson's disease. These results illustrate the necessity of taking therapeutic measures into account in the interpretation of data on aminotransferase activities.
Wien Klin Wochenschr 1975 Dec 12
PMID:[The activity of aminotransferases in serum and cerebrospinal fluid in neurological diseases (author's transl)]. 12 63

Because it is commonly believed that acetylcholine is a synaptic transmitter in the caudate nucleus and that the reduction of striatal biogenic amines in Parkinson's disease leads to acetylcholine supersensitivity in the caudate nucleus, we investigated the effects of the muscarinic blocking agent scopolamine on synaptic responses of neurons in the intact feline caudate nucleus and in the caudate nucleus depleted of dopamine by long-standing nigrostriatal lesions. In the intact caudate nucleus, micro-iontophoretic application of scopolamine selectively blocked the neuronal responses to stimulation of the caudate nucleus near the recording site without affecting the responses to stimulation of the sensorimotor cortex or the substantia nigra in the same fashion. This suggests that acetylcholine is a synaptic transmitter of caudate interneurons. Responses to thalamic stimuli were also blocked by scopolamine, suggesting that acetylcholine may be a transmitter of thalamic afferents although the course of these afferents is unclear. In the dopamine-depleted caudate nucleus scopolamine was more effective than in the intact caudate nucleus blocking the neuronal responses to stimulation of the caudate nucleus. This greater blocking effect by scopolamine suggests an increased effect of endogenous acetylcholine in this response and supports previous observations of an increased excitatory effect of iontophoretic acetylcholine in the dopamine-depleted caudate nucleus. These results suggest that the acetylcholine supersensitivity which follows nigrostriatal degeneration may be due to increased effectiveness of synaptic transmission by cholinergic interneurons in the caudate nucleus.
Brain 1978 Dec
PMID:Selective blockade by scopolamine of synaptic responses in cat's caudate nucleus and its modification by lesions of the substantia nigra. 21 58

Parkinson's disease, 'paralysis agitans', is characterized by a number of abnormalities. A similar clinical picture may be symptomatic of other disturbances: these are briefly described and the differential diagnosis is discussed.
Postgrad Med J 1977 Dec
PMID:Symptomatic Parkinsonism. 34 78


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