Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The unilateral microinjection of ACTH 1-24 (20 nmol) into the locus coeruleus (LC) produced a long lasting (2-3 hr) posture asymmetry and movement disorder in all rats tested. This response was readily suppressed by the subsequent local microinjection of an equimolar dose of beta-endorphin or morphine or by the intraperitoneal injection of morphine sulphate (50 mg/kg). Microinjection of naloxone (20 nmol) into the LC produced the above syndrome in a lower percentage of animals. The results support the hypothesis that ACTH peptides and opioids play opposite roles in the control of different brain functions.
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PMID:Morphine and beta-endorphin antagonize posture and locomotor disorders induced by the injection of ACTH 1-24 in the rat locus coeruleus. 300 78

A search for the defective gene causing torsion dystonia has been carried out in a family manifesting an autosomal dominant mode of inheritance of this movement disorder. Complete neurologic examination and establishment of lymphoblast lines have been carried out for over 50 members. Linkage analysis, using cloned DNA sequences and restriction fragment length polymorphisms, was evaluated by the LOD score method with requisite assumptions for mode of inheritance, age-of-onset and incomplete gene penetrance. Genes for pro-opiomelanocortin and glutamic acid decarboxylase, which have been implicated in the etiology of the disease in rat models, were excluded as being responsible for the disease state in this family. Other regions of the genome were also excluded using DNA probes for other genes and random "unique" sequences.
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PMID:Linkage analysis in a family with dominantly inherited torsion dystonia: exclusion of the pro-opiomelanocortin and glutamic acid decarboxylase genes and other chromosomal regions using DNA polymorphisms. 301 20

A unilateral microinjection of adrenocorticotropin 1-24 in the rat brainstem in the region of the locus ceruleus resulted in postural asymmetry and movement disorder that resembled human dystonia, the severity and duration (2 to 3 days) being dose-dependent. These results show for the first time that neuropeptides in the brainstem may modulate posture and movement, and they suggest that some forms of movement disorder such as dystonia may be due to a disordered regulation of postural and locomotor mechanisms by adrenocorticotropin 1-24.
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PMID:Postural asymmetry and movement disorder after unilateral microinjection of adrenocorticotropin 1-24 in rat brainstem. 628 33

Huntington's disease is a progressive degenerative neurological disorder which produces a characteristic movement disorder termed chorea. Although chorea is associated with dysfunction of the basal ganglia, the underlying mechanisms by which dyskinesias such as chorea are produced, are poorly understood. Recent studies in primates have led to experimental models of chorea with postulated involvement of specific neural pathways. In the present study we attempted to determine the validity of the experimental models by measuring concentrations of gamma-aminobutyric acid (GABA), glutamate, substance P and met-enkephalin in the basal ganglia of Huntington's disease patients who manifested either chorea or rigidity/bradykinesia within 6 months of death. We also characterized changes in the Huntington's disease patients according to pathological grade, since this may be a confounding factor. We analysed post-mortem brain tissue from 12 controls, and 11 grade 3 and 12 grade 4 Huntington's disease patients. The grade 3 and 4 cases consisted of eight adult-onset choreic, nine adult-onset rigid and six juvenile-onset rigid patients. We also analysed the putamen and globus pallidus from 11 grade 2 adult onset choreic Huntington's disease patients. A model of chorea based on experimental studies in primates proposes that a loss of striatal GABAergic inhibitory projections to the globus pallidus externa leads to increased activity of the inhibitory globus pallidus externa GABAergic neurons which project to the subthalamic nucleus. It is believed that the loss of GABAergic inputs to the globus pallidus externa precedes a loss of GABAergic input to the globus pallidus interna, which occurs later in the disease and is associated with the development of rigidity and bradykinesia. In the choreic Huntington's disease patients whom we studied, there was a greater loss of GABA in the globus pallidus externa than in the globus pallidus interna, and the globus pallidus interna: globus pallidus externa GABA ratio was significantly increased compared with rigid patients. There were also increases in GABA in the subthalamic nucleus in the choreic patients, although this did not reach significance. A differential loss of met-enkephalin in the globus pallidus externa compared with substance P loss in the globus pallidus interna was not observed in either the choreic patients with advanced disease or the grade II patients. There was a significant increase in GABA concentrations in the ventroanterior nucleus of the thalamus in the choreic patients compared with rigid/bradykinetic patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurochemical substrates of rigidity and chorea in Huntington's disease. 769 98

Movement disorders associated with multiple sclerosis (MS) are uncommon, except for tremor. We report two patients with relapsing-remitting MS, who developed either dystonia or chorea during clinical exacerbation of their MS. The movement disorders resolved during treatment with adrenocorticotropin hormone (ACTH). Acute exacerbations of MS may be associated with transient movement disorders, which are responsive to ACTH.
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PMID:Transient movement disorders and multiple sclerosis. 1247 1

The aim of this study was to evaluate demographic and polysomnographic characteristics of positional (PPJ) and non-positional obstructive (NPP) sleep apnea (OSA) patients in 2077 OSA patients diagnosed in our Sleep Disorders Unit during a period of 10 years. An OSA patient is defined as positional if he has twice as many or more breathing abnormalities (apnea and hypopneas) while he sleeps in his supine posture compared to the lateral ones. Of the 2077 OSA patients, 1118 (53.8%) were positional and 959 (46.2%) were non-positional. No age differences were found between these two groups of patients. However, NPP were heavier and thus had a higher BMI than PP. PP had fewer and Less severe breathing abnormalities during sleep compared to NPP and thus, they enjoyed better sleep quality expressed by higher percentages of stage 2, 4 and 3+4 as well as a lower amount of short arousals than NPP. Also, PP patients are less sleepy during daytime hours than NPP. During the Multiple Sleep Latency Test (MSLT), NPP fall asleep faster in every nap than PP patients. No differences between these two patient groups were found for any parameter of Periodic Limb Movement Disorders. AHI and BMI are independently but inversely related to positional dependency. As AHI and BMI increase, the Likelihood to be a positional patient decreases. NPP have breathing abnormalities in the supine and lateral postures, thus, for them without question, CPAP is the treatment of choice. Since avoiding the supine posture during sleep may significantly improve the sleep quality and daytime alertness of many positional patients, it is imperative to carry out a high-quality study to evaluate if this is a real therapeutic alternative for many positional patients.
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PMID:[The significance of body posture on breathing abnormalities during sleep: data analysis of 2077 obstructive sleep apnea patients]. 1963 Mar 60

Non-pharmacologic treatments of Sleep-Related Movement Disorders (SRMD) are already well described in the literature. The physical activity has been presented as a factor to improve quality of life and in several aspects related to sleep disorders. Thus, the purpose of this review was to analyze the benefits of physical exercise and your indication to improve to SRMD. In the research, 19 studies were found that evaluate the efficacy of physical exercise on SRMD in both human and animal models. The results demonstrate that both acute and chronic physical exercises are effective in reducing symptoms of SRMD. However, most studies were performed with aerobic exercise. Three studies evaluated the efficacy of combined exercise, and no studies have investigated the relationship of resistance exercise. Regarding the mechanisms involved, a study discusses the relationship between the release of beta-endorphin and the exercise practice, and two studies with animal models show the changes of the dopaminergic system after physical exercise. From this evidences, we suggested that physical exercise is a favorable non-pharmacological treatment for SRMD. However, more studies should be available for a better understanding of the molecular mechanisms involved, as well of the type, duration and better time of the day to practice.
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PMID:Exercise as a favorable non-pharmacologic treatment to Sleep-Related Movement Disorders: a review. 3187 45