Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tripeptide, prolyl-leucyl glycine amide, a melanocyte-stimulating hormone inhibitory factor (MIF-I), which has been reported to be effective in improving symptoms of Parkinson's disease, has been compared with drugs known to activate dopamine receptors in rat and mouse brain. Unlike apomorphine, amphetamine and amantadine it was incapable of producing sterotyped behaviour in the rat and unlike 1-dopa it was also ineffective in rats pretreated with the monoamineoxidase inhibitor mebanazine. Neither did it potentiate apomorphine nor amphetamine in this test. MIF-I did not antagonise chlorpromazine-induced loss of locomotor activity in mice, an effect which was antagonised by apomorphine, amphetamine and amantadine. Chlorpromazine hypothermia in the mouse was antagonised by 1-dopa but not by MIF-I; similar findings were obtained in reserpine-pretreated mice. These results suggest that the reported beneficial effect of MIF-I in Parkinson's disease is unlikely to be due to an interaction with dopamine systems in the brain.
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PMID:A comparison between a melanocyte-stimulating hormone inhibitory factor (MIF-I) and substances known to activate central dopamine receptors. 0 32

In eight subjects with Parkinson's disease under an optimal daily dose of L-dopa, acute administration of MIF-I (200 mg i.v.) did not ameliorate either the total disability score or the intellectual test PM 38 when evaluated in comparison with the effect induced by acute administration of a placebo. Also concomitant evaluation of the effect of MIF-I on the secretion of anterior pituitary hormones which are under dopaminergic control i.e., growth hormone and prolactin, did not reveal any potentiation of the L-dopa-induced stimulus.
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PMID:Failure of MIF-I to affect behavioral responses in patients with Parkinson's diseases under L-dopa therapy. 3 8

This review evaluates the long-term results of Levodopa therapy in Parkinson's disease upon quality of life, prolongation of survival and excess mortality. It also focuses on recent and new therapeutic approaches: Levodopa in combindation with a Dopa-decarboxylase inhibitor or MAO-B inhibitor, dopamine agonists and an active tripeptide: L-prolyl-L-leucylglycine amide (MIF-I). It ends by looking at new avenues of etiological research in Parkinson's disease which may indicate specific accelerated ageing of catecholaminergic (pigmented) neuronal systems.
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PMID:Progress in understanding and treating Parkinson's disease. 77 22

A number of questions remain unsettled about the release of melanocyte-stimulating hormone (MSH) and about its function. Even though relatively few investigators are studying this area, some generalities have emerged during the last 10 years. It now seems that release of MSH from the pituitary is inhibited by a substance present in the hypothalamus. The structure of this physiologic inhibitor of MSH release may still not be considered an established entity but there is evidence for additional mechanisms capable of exerting a fine control on the release of MSH. Contrary to some opinions, the release of MSH does not always occur together with the release of ACTH, and the release of the two hormones can be dissociated in several laboratory and clinical situations. In addition, many studies have shown that the pituitary peptide, MSH, exerts behavioral and electroencephalographic effects in both the rat and man. The hypothalamic peptide Pro-Leu-Gly-NH2 (MIF-I) also has direct effects on the central nervous system that may include alleviation of the symptoms of Parkinson's disease.
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PMID:Some questions related to melanocyte-stimulating hormone. 96 14

The changes of the contents of enkephalins in cerebrospinal fluid (CSF) and the action of MIF-1 in rabbit experimental models of Parkinson's disease were studied. In the experiment, the rabbits received injection of 6-hydroxydopamine (6-OH DA) into the unilateral substantia nigra. The contents of Met-enkephalin (MEK) and Leuenkephalin (LEK) in the CSF of the fourth ventricles of the normal control rabbits and those with destructive lesions in the substantia nigra were determined with radio-immunoassay. The concentrations of MEK and LEK in CSF of the rabbit models increased markedly to 14.3 and 28.2 folds in the controls respectively. The increased enkephalin content in CSF could be reduced to the normal level by intravenous administration of MIF-I. The results indicated that the action of MIF-I may be one of the important factors in alleviating the symptoms of parkinsonian patients.
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PMID:[An experimental study on the contents of enkephalins in the cerebrospinal fluid in rabbits with unilateral destructive lesions produced in the substantia nigra and their relation to the regulation of MIF-1]. 257 67