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)

Fenfluramine therapy has been reported to improve behavior in infantile autism and has been associated with a decrease in abnormally increased blood serotonin content. The primary central effect has not been proved to be serotonergic. Beta-endorphin is involved in the anorexic effect of fenfluramine and may play a role in autism. Nine children with infantile autism were treated with fenfluramine in double-blind, placebo-crossover design. Transient anorexia was the only adverse effect. Autistic behavior was reported to improve in three patients, but objective psychometric tests were unchanged. Beta-endorphin-like immunoreactivity was determined in lumbar cerebrospinal fluid of patients during and before or after treatment with fenfluramine and then was compared to normal controls. Beta-endorphin was elevated significantly in the baseline autistic group (p less than .005) and was reduced toward control values during fenfluramine treatment. The results are consistent with a role for beta-endorphin in infantile autism and in the mechanism of fenfluramine treatment.
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PMID:Reduction of elevated CSF beta-endorphin by fenfluramine in infantile autism. 297 80

Due to asymmetry of brain neurotransmitters and differential hemispheric information processing modes, it is suggested that the excessive use of one information processing mode could engender a state of brain reactivity whose neurochemical correlates would be either a rise in melatonin or beta-endorphin in systemic circulation. Since melatonin and beta-endorphin have opposite effects on lung-mediated regulation of prostaglandins, it is further suggested that the pulmonary inactivation of prostaglandin E1 would either be increased or inhibited. Low levels of PGE1 would engender high levels of PGE2 whose effects would explain the findings in schizophrenics of: 'reducing' pattern of visual evoked response, cerebral atrophy, and viral and autoimmune phenomena. The primacy of the disordered cognitive style in leading up to the immunological, biochemical and neuropathological processes is stressed. Implications of this model for understanding depression, anxiety and phobic disorders, autism, attention deficit disorder, obesity, alcoholism, smoking, drug addiction, sexual deviations, and certain psychosomatic and psychophysiological disorders are suggested.
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PMID:How information processing mode could affect prostaglandin E1 metabolism and lung inactivation: relevance of hemispheric specialization, neurotransmitter asymmetry and brain reactivity. 614 17

To investigate pediatric brain impairment, beta-endorphin levels, one of the opioid peptides that modulate human high cortical functions, were measured in cerebrospinal fluid (CSF). The study included 19 patients with infantile autism, 3 patients with Rett syndrome, 6 patients with infantile spasms, 16 patients with aseptic meningitis, and 23 age-matched controls. In the control group, the CSF beta-endorphin concentrations were negatively correlated with increasing age. There was no correlation between body temperature and the levels, and no significant difference in the levels according to sex. In infantile autism, the CSF level was not significantly different from that in controls. In Rett syndrome, it was significantly higher, while in infantile spasms it was lower than in controls. In aseptic meningitis, the CSF beta-endorphin level was significantly higher than in controls. The alterations in CSF beta-endorphin levels may play a role in these neurologic disorders and/or in central nervous system (CNS) infections.
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PMID:CSF beta-endorphin levels in pediatric neurologic disorders. 800 32

The emerging concept of opioid peptides as a new class of chemical messengers of the neuroimmune axis and the presence of a number of immunological abnormalities in infantile autism prompted us to correlate biological (hormonal and immunological) determinations and behavioural performances during treatment with the potent opiate antagonist, naltrexone (NAL). Twelve autistic patients ranging from 7 to 15 years, diagnosed according to DSM-III-R, entered a double-blind crossover study with NAL at the doses of 0.5, 1.0 and 1.5 mg/kg every 48 hours. The behavioural evaluation was conducted using the specific BSE and CARS rating scales NAL treatment produced a significant reduction of the autistic symptomatology in seven ("responders") out of 12 children. The behavioural improvement was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase of the T-helper-inducers (CD4+CD8-) and a significant reduction of the T-cytotoxic-suppressor (CD4-CD8+) resulting in a normalization of the CD4/CD8 ratio. Changes in natural killer cells and activity were inversely related to plasma beta-endorphin levels. It is suggested that the mechanisms underlying opioid-immune interactions are altered in this population of autistic children and that an immunological screening may have prognostic value for the pharmacological therapy with opiate antagonists.
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PMID:Opioid-immune interactions in autism: behavioural and immunological assessment during a double-blind treatment with naltrexone. 902 57

We measured CSF levels of beta-endorphin, an opioid hormone, in 19 patients with infantile autism and in 3 patients with Rett syndrome, and compared them with control values. In infantile autism, CSF levels of beta-endorphin did not differ significantly from those of age-matched controls. There was no significant correlation between CSF levels and clinical symptoms, including self-injurious behavior, pain insensitivity, and stereotyped movement. However, CSF levels of beta-endorphin were significantly higher in the patients with Rett syndrome than in the control (p < .05). Data suggest that neurons containing beta-endorphin may not be involved in patients with infantile autism. Thus, there is no relationship between dysfunction of brain opioid and autism.
J Autism Dev Disord 1997 Apr
PMID:CSF beta-endorphin levels in patients with infantile autism. 910 66

Plasma levels of the hypothalamo-pituitary-adrenal axis hormones beta-endorphin (BE), adrenocorticotropin hormone (ACTH), and cortisol were measured in autistic (N = 48), mentally retarded/cognitively impaired (MR/CI, N = 16), and normal control (N = 26) individuals. Comparison of log transformed data from the three groups revealed that levels of BE and ACTH were significantly higher (p < .05) in the autistic individuals than in normal controls. The higher means in the autistic group were due to significantly higher plasma levels of BE and ACTH, indices of acute stress response, in the more severely affected individuals. The data support the idea that individuals with severe autism have a heightened response to acute stressors rather than chronic hyperarousal or elevated basal stress response system functioning.
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PMID:Plasma beta-endorphin, adrenocorticotropin hormone, and cortisol in autism. 931 80

Self-injurious behavior (SIB) is an untreatable and often life-threatening problem among individuals with developmental disorders, especially those diagnosed with autism. Functioning, relationships and processing of the proopiomelanocortin (POMC) system are "uncoupled" in subgroups of self-injuring individuals resulting in different ratios of ACTH and opioids in the bloodstream, particularly under conditions of stress. In this study, relations between SIB and POMC were evaluated in a multi-year study of the largest prospective sample studied to date. Observations were collected on palmtop computers for 45 treatment-resistant patients who exhibited chronic SIB. Behavior of each subject was observed in natural settings without disruption or intrusion, for continuous, 2.5-h periods, two times a day (morning and afternoon), 4 days a week for two consecutive weeks, for a total of 40 h/subject. Blood was collected in the morning, late afternoon and immediately after an SIB episode on two separate occasions separated by at least 6 months. Levels of beta-endorphin (beta E) and ACTH were assayed by RIA. We discovered that the SIB was the best predictor of subsequent SIB. Moreover, the majority of subjects exhibited this contagious pattern of SIB. Levels of POMC fragments were reliable over a 6- to 9-month period. Subjects exhibiting POMC disregulation characterized by high morning levels of beta E had the highest transitional probabilities of SIB (i.e. contagious patterns; F=8.17, P<0.01). These findings suggest that subjects with "contagious" SIB may represent a behavioral phenotype associated with disregulated expression of the POMC gene.
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PMID:Disregulation of proopiomelanocortin and contagious maladaptive behavior. 1222 Jul 43

The objective of this study was to compare the efficacy of corticotropin (ACTH) versus vigabatrin in treating infantile spasms and to determine which medication has a more favorable long-term outcome in terms of cognitive function, evolution of epilepsy, and incidence of autism. Patients with infantile spasms were included in the study if they were 3 to 16 months old, had hypsarrhythmia, and had no previous treatment with vigabatrin or corticosteroids. Patient evaluation included electroencephalographic and psychometric measures before and after treatment. Patients were stratified based on etiology (idiopathic or symptomatic) and sex and then randomized between the ACTH and vigabatrin treatment groups. Each of the treatment groups received either ACTH or vigabatrin for 2 weeks. At the end of 2 weeks of treatment, patients were considered responders if spasms and hypsarrhythmia resolved. Nonresponders were crossed over and treated with the alternate drug. Nine patients were included in the study. Three patients received ACTH, one of whom was a responder. Six patients received vigabatrin, three of whom were responders. The five nonresponders received both therapies. All patients had some degree of developmental plateau or regression before the initiation of treatment. Four patients with idiopathic infantile spasms showed improved cognitive function following treatment. The remaining five patients remained significantly delayed. Five patients with symptomatic infantile spasms had epilepsy following treatment; three of them were in the autistic spectrum. The small number of infants in this pilot study is insufficient to determine which of the two drugs is more effective. However, the following trends were identified: vigabatrin may be more effective for patients with symptomatic infantile spasms; patients with idiopathic infantile spasms tend to have a better cognitive outcome; and patients with symptomatic infantile spasms tend to develop both epilepsy and autism.
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PMID:Prospective preliminary analysis of the development of autism and epilepsy in children with infantile spasms. 1273 40

Blood concentrations of pituitary hormones adrenocorticotropin (ACTH), prolactin, growth hormone, and adrenal hormone-cortisol were measured in 36 autistic and 27 control individuals. Individuals with autism had significantly lower serum concentrations of cortisol (p < 10(-6)), and significantly higher concentrations of ACTH (p = 0.002) than control age- and sex-matched subjects. Also, prolactin concentrations in autistic patients with epilepsy were significantly higher when compared with normal subjects. The observed hormonal changes may indicate dysfunction of the hypothalamo-pituitary-adrenal axis in individuals with autism.
J Autism Dev Disord 2003 Aug
PMID:Lower cortisol and higher ACTH levels in individuals with autism. 1295 23

Brain asymmetry is understood as an anatomical, functional or neurochemical difference between the two hemispheres. It is not a static but rather a dynamic phenomenon in which both environmental and endogenous factors act as modulators. Aging modifies brain asymmetry, and an imbalance in specific asymmetries characterizes some brain disorders such as schizophrenia, depression, infantile autism or Alzheimer's disease. However, it is not clear whether these changes are a cause or a consequence of these disorders. Although this phenomenon has been extensively studied, its functional significance is not yet clear, and the neurochemical basis underlying anatomical or functional asymmetries in the brain is still poorly understood. In recent decades intensive research on the behaviour of neuropeptides has revealed asymmetries in their distribution in the brain, and there is evidence that the lateralized patterns of distribution are involved in the regulatory control of some neuropeptidase activities. Therefore, if these enzymatic activities are distributed asymmetrically, their endogenous substrates would presumably be affected in an asymmetrical way, as would the functions they are involved in. Here we review the most significant literature regarding human and animal brain asymmetry involving neuropeptides such as corticotropin-releasing hormone, cholecystokinin, luteinizing hormone-releasing hormone, thyrotropin-releasing hormone and angiotensin II, as well as their neuropeptidases.
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PMID:Neuropeptides, neuropeptidases and brain asymmetry. 1558 19


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