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)

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

Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the central nervous system, and diseases that associate a deficiency in GABA might benefit from GABAergic drugs. Cerebellar Purkinje cells employ GABA as a neurotransmitter. Cortical cerebellar atrophy (CCA) shows Purkinje cell loss, and ataxia caused by it was alleviated by gabapentin and pregabalin. Thus, CCA is proposed as a model of selective deficiency in GABA in the cerebellum, which benefits clinically from administration of GABAergic drugs, in a manner similar in which levodopa improves motor manifestations in Parkinson's disease. Other ataxias also benefited clinically from GABAergic drugs, as adult-onset GM2 gangliosidosis, olivopontocerebellar atrophy, cerebellar ataxia with hypogonadism, spinocerebellar ataxias 1, 2 and 6, and adult-onset ataxia-telangiectasia. Complex neurochemical diseases, as multiple-system atrophy, had ataxia worsened by GABAergic drugs. Various disorders with a deficiency in GABA content had their manifestations relieved by admistration of GABAergic drugs, as one patient with progressive encephalomyelitis with rigidity, whose muscular spasms were suppressed by a combination of gabapentin and tiagabine, and another with diaphragmatic myoclonus, who required gabapentin and tiagabine for symptomatic control. On the contrary, GABAergic drugs were not effective in cervical dystonia, amyotrophic lateral sclerosis, Parkinson's disease and progressive supranuclear palsy, presumably because a deficiency in GABA is not an essential neurochemical abnormality in these diseases. Research aimed at identifying effective therapies to treat cerebellar ataxias and other motor disorders of the central nervous system is warranted. Meanwhile, therapeutic tests with GABAergic drugs might yield clinical improvement in these diseases.
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PMID:GABAergic Pharmacotherapy in the Treatment of Motor Disorders of the Central Nervous System. 2636 42