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)

Altered prolactin and thyrotropin responses to the TRH test in parkinsonian patients are held to indicate an impairment of the tubero-infundibular dopaminergic axis (TIDA). We correlated the plasmatic prolactin (PRL), thyrotropin (TSH) and somatotropin (GH) responses to TRH and bromocriptine + TRH of 12 parkinsonian patients, who had never received anti-parkinsonian drugs, with the severity, the duration, the age of onset and the dopamine-dependence of the motor symptomatology as indicated by the therapeutic response to a six-month oral treatment with bromocriptine. Patients with basal motor impairment over 9 on the Webster Rating Scale (WRS), those with duration of the disease over 24 months and those with onset earlier than 55 years of age showed lower PRL responses than the respectively matched subgroups. Patients showing a therapeutic motor improvement over 50% on the WRS (dopamine-dependent or "responder") showed lower PRL and TSH and higher GH responses than the non-responders. These findings suggest that the TIDA impairment described in Parkinson's disease develops along with the progressive course of the extrapyramidal involvement and is strictly correlated with the dopamine-dependence of the motor impairment.
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PMID:Hypothalamo-pituitary function and dopamine dependence in untreated parkinsonian patients. 190 36

Amantadine, a well-known antiviral agent, causing an increase in dopamine synthesis, release and the inhibition of re-uptake of noradrenaline and dopamine in central and peripheral catecholaminergic neurons, is successfully used in the treatment of Parkinson's disease. In the present paper, we have studied the effect of various doses of amantadine on in vivo prolactin secretion and the incorporation of 3H-thymidine and 3H-spiperone binding by the anterior pituitary gland of long-term diethylstilboestrol-treated male Wistar rats. Four weeks after a subcutaneous implantation of Silastic tubes containing 10 mg of diethylstilboestrol, a dramatic rise in serum prolactin levels was observed, accompanied by an increased uptake of 3H-thymidine by DNA anterior pituitary cells. Amantadine, given in the subcutaneous doses of 50, 5 and 0.5 mg/kg of body weight attenuated the stimulatory effect of stilboestrol on serum prolactin concentration in a dose-dependent fashion. On the other hand, the incorporation of 3H-thymidine into DNA pituitary cells in all the groups of amantadine-treated rats was only slightly suppressed. In an additional experiment, Scatchard analyses were performed on the in vitro 3H-spiperone binding kinetics in a dispersed anterior pituitary cell culture prepared from the pituitaries of 6-week diethylstilboestrol-treated rats. It has been found that amantadine injected in the dose of 5 mg/kg of body weight for 14 days induced a twofold decrease in the density of dopamine D2 binding sites (36.6 +/- 9.4 vs. 70.3 +/- 3.4 fmol/10(6) cells; p less than 0.02), while the apparent affinity of the receptors was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of amantadine on prolactin secretion, pituitary DNA synthesis and 3H-spiperone binding in male estrogen-treated rats. 214 19

1. Cysteamine is formed by degradation of coenzyme A (CoA) and causes somatostatin (SS), prolactin and noradrenaline depletion in the brain and peripheral tissues. 2. Cysteamine influences several behavioral processes, like active and passive avoidance behavior, open-field activity, kindled seizures, pain perception and SS-induced barrel rotation. 3. Cysteamine has several established (cystinosis, radioprotection, acetaminophen poisoning) and theoretical (Huntington's disease, prolactin-secreting adenomas) indications in clinical practice. 4. Pantethine is a naturally occurring compound which is metabolized to cysteamine. 5. Pantethine depletes SS, prolactin and noradrenaline with lower efficacy compared to that of cysteamine. 6. Pantethine is well tolerated by patients and has been suggested to treatment of atherosclerosis. The other possible clinical indications (alcoholism, Parkinson's disease, instead of cysteamine) are discussed.
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PMID:Preclinical and clinical studies with cysteamine and pantethine related to the central nervous system. 227 50

Among 49 consecutive patients with Parkinson's disease, 40% were depressed according to DSM-III; they had major depression or dysthymic disorder accompanied by sleep disturbance, fatigue, psychomotor retardation, loss of self-esteem, and excessive guilt. During a 10-day dopamine-free period, lumbar puncture was performed to measure the metabolites of dopamine, serotonin, and norepinephrine. Patients were given an overnight dexamethasone suppression test, and the effects of thyrotropin-releasing hormone and L-dopa on plasma growth hormone and prolactin were examined. Level of CSF 5-hydroxyindoleacetic acid was lowest in parkinsonian patients with major depression and was related to psychomotor retardation and loss of self-esteem.
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PMID:Clinical and biochemical features of depression in Parkinson's disease. 242 23

Somatostatin (SRIF) actions in the brain and pituitary are mediated by specific receptors. Using radioiodinated ligands it has been possible to characterize the kinetics of specific binding sites in the brain and pituitary, and to determine their cellular localization by autoradiography. At the pituitary level, the inhibition of growth hormone, prolactin and thyrotropin secretions induced by SRIF is mediated through a single binding site which is coupled to the inhibition of adenylate cyclase. In the brain, SRIF receptors are localized on neurons and glial cells and are also coupled to adenylate cyclase inhibition. Two sites are differentiated in the brain with an analogue of somatostatin, SMS 201995. In humans, SRIF-binding sites have been related to a number of pathologies. At the pituitary level, it has been shown that the number of binding sites was negatively correlated to growth hormone levels in acromegaly. Furthermore, SRIF-binding sites were undetectable in a patient which did not respond to SMS 201995 therapy. In the brain, meningiomas and gliomas are rich in SRIF binding sites. This suggests a possible role for SRIF on glia. In neurodegenerative diseases, cortical SRIF concentrations are decreased in Alzheimer's and Parkinson's disease associated with dementia while SRIF-binding sites are only affected in Alzheimer's disease. In conclusion, the physiological role of SRIF in the brain and pituitary can be evaluated by studying the receptors of the peptide. Such studies allow to question the implication of SRIF in endocrine and neuropathologies.
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PMID:Somatostatin receptors in brain and pituitary. 256 73

The neuroendocrine function is regulated by several neurotransmitters (acetylcholine, dopamine, somatostatin and noradrenaline) known to be reduced in brains of patients with Alzheimer's disease (AD). Moreover, the hypothalamus also has pathological changes. In spite of these findings suggesting neuroendocrine dysfunctions, this function has seldom been investigated in AD patients so far. We have compared patients with clinically 'probable' AD of mild-to-moderate severity with nondemented age- and sex-matched controls. Plasma levels of prolactin (PRL), growth hormone (GH) and thyroid-stimulating hormone (TSH) were measured by commercially available radioimmunoassays (RIA) before and after stimulation with metoclopramide, l-dopa or thyrotropin-releasing hormone. Basal plasma levels of beta-endorphin and beta-lipotropin were measured by RIA after high-performances liquid chromatography. Basal and stimulated plasma levels of PRL, GH, TSH and beta-lipotropin were similar in the two groups. Basal lamina levels of beta-endorphin were significantly higher in the patient group. Of doubtful clinical importance, this might be attributed to decreased tuberoinfundibular dopaminergic activity and has also been seen in patients with Parkinson's disease.
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PMID:Neuroendocrinological function in Alzheimer's disease. 297 29

Bromocriptine, or 2-bromo-alpha-ergocryptine, is a semisynthetic ergot alkaloid. The basis of its therapeutic application in endocrine and neurological diseases is its action as a potent dopamine agonist. Its ability to inhibit prolactin secretion has led to its successful use in suppression of puerperal lactation and in the treatment of pathological hyperprolactinaemia causing galactorrhoea, infertility or hypogonadism. It has been shown to be safe in pregnancy. The ability of bromocriptine to reduce the size of large prolactin-secreting pituitary tumours has resulted in the recovery of pituitary function and correction of visual field defects. Bromocriptine is less effective in acromegaly but is useful as adjuvant therapy to radiotherapy and/or surgery which has been the standard mode of treatment. It has been shown to be efficacious either alone or in combination with levodopa in the treatment of Parkinson's disease. Therapy with low doses appears to be effective and is associated with a significantly reduced incidence of side effects. The successful use of bromocriptine has also been reported for the treatment of non-functioning pituitary tumours, premenstrual syndrome, cyclical mastalgia, luteal phase insufficiency and portal-systemic encephalopathy, although its role in the treatment of these latter disorders remains uncertain until more extensive and adequately controlled trials have been conducted.
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PMID:Therapeutic applications of bromocriptine in endocrine and neurological diseases. 306 95

In 64 patients with Parkinson's disease (PD), the basal level of prolactin (PRL) was normal. Bromocriptine (BCT) caused a significant suppression of PRL in all parkinsonian patients and controls. When given after BCT treatment, thyrotropin-releasing hormone (TRH) induced a significantly lower PRL rise in recent-onset parkinsonian patients than in controls or advanced patients. In advanced parkinsonian patients with daily fluctuations in disability, the corresponding TRH-induced PRL response was significantly higher than in controls. In advanced parkinsonian patients without fluctuations, the PRL response to TRH was almost the same as in controls.
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PMID:Function of dopamine receptors in Parkinson's disease: prolactin responses. 308 30

Thirteen drug-free and not severely affected patients with idiopathic Parkinson's disease underwent an insulin-hypoglycaemia test, a TRH test and a levodopa test. The responses of growth hormone, prolactin, cortisol and thyrotropin were measured, and retested under stable therapy with levodopa and benserazide. Mean basal and stimulated hormonal concentrations were in the normal range before and during therapy. Minor abnormalities were observed in individual cases, but did not indicate a hypothalamic dopamine deficit.
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PMID:Effect of hypoglycaemia, TRH and levodopa on plasma growth hormone, prolactin, thyrotropin and cortisol in Parkinson's disease before and during therapy. 308 17

A deficit of nigrostriatal, mesocortical and mesolimbic dopamine systems in Parkinson's disease is well known. We know less about the involvement of tuberoinfundibular dopamine (TID) systems. In untreated (naive or wash-out) men with Parkinson's disease, we studied TID function through basal and stimulated plasma levels of growth hormone, prolactin and thyrotropin. Only minor abnormalities in prolactin responses to thyrotropin-releasing hormone were found, probably reflecting denervation hypersensitivity. TID function is preserved in men with Parkinson's disease.
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PMID:Tuberoinfundibular dopaminergic function in Parkinson's disease. 313 13


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