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)

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

Rett syndrome (RS) is a progressive disorder that is predominant in females. It is associated with cortical atrophy, stereotyped hand movements mimicking hand-washing, severe mental deficiency, and cortical and extrapyramidal dysfunction. The cause of RS is unknown; no consistent genetic abnormalities, at either the cellular or mitochondrial levels, have been identified. The diagnosis still depends solely upon clinical evidence. The clinical progression of RS is consistent with an arrested neuronal development that may be due to either impaired cellular differentiation or the lack of appropriate trophic factors. Neuropathological studies have confirmed (1) a generalized brain atrophy involving the cerebrum and cerebellum; (2) a decrease in neuronal cell size and increased cell packing density throughout the brain; (3) a reduction in the number of basal forebrain cholinergic neurons; (4) a reduction in the concentration of melanin-containing neurons in the substantia nigra. Biochemical studies have identified (1) a decrease in cholinergic markers in the neocortex, hippocampus, thalamus and basal ganglia; (2) inconsistent and variable changes in biogenic amine biomarkers in post-mortem tissues and cerebrospinal fluid (CSF); (3) an elevation of beta-endorphin levels in the thalamus and glutamate levels in the CSF; (4) no evidence for mitochondrial dysfunction. These data suggest that there is a primary deficit in cholinergic function that might underlie some of the higher cognitive impairments and extrapyramidal dysfunction. Overall, the clinical, biochemical and neuropathological data suggest that RS is a neurodevelopmental disorder that has its greatest effects upon a limited number of neural systems during the first few years of postnatal life.
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PMID:Rett syndrome: neurobiological changes underlying specific symptoms. 910 98

The known interaction between the immune system and the hypothalamic-pituitary-adrenal axis led us to explore the interrelation between magnetic resonance imaging findings and the hypothalamic-pituitary-adrenal axis activity in 53 multiple sclerosis patients. The cortisol release induced by the dexamethasone-corticotropin-releasing hormone test was negatively associated with the presence and number of gadolinium-enhancing lesions and positively associated with ventricular size. This finding suggests a protective effect of the hypothalamic- pituitary-adrenal drive on acute lesional inflammation in multiple sclerosis, probably by limiting immune overshoot. In contrast, the nature of the correlation between hypothalamic-pituitary-adrenal hyperdrive and brain atrophy remains to be determined.
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PMID:Activity of the hypothalamic-pituitary-adrenal axis in multiple sclerosis: correlations with gadolinium-enhancing lesions and ventricular volume. 1211 83

At its final meeting, the MS Forum Executive Committee reviewed highlights of where things stood prior to the immunomodulatory era, and how things have evolved subsequently. What the future might hold was discussed in a second session. Prior to 1990: Genetic predisposition to multiple sclerosis (MS), as determined by human leukocyte antigen expression, was established and an environmental trigger (Epstein-Barr virus?) was suspected, as was lack of sunshine. Substantial evidence for activated T-cells as relapse initiators had accumulated. Defective regulatory cell function that correlated with disease activity was shown. Adrenocorticotropic hormone lessened relapse severity as did its steroid replacement. A trial of cyclosporine, a T-cell inhibitor, in progressive MS failed. The drug, not the patients chosen, was blamed. 1990-2010: Approval of interferon-beta (IFNB)-1b was followed promptly by IFNB-1a, glatiramer acetate, mitoxantrone and then by natalizumab and fingolimod. All reduce MS attack frequency and new lesion accumulation. None have reduced disability progression in progressive MS. Brain atrophy, cognitive loss and axonal interruption in progressive MS depend on innate immune system activation rather than on T-cells. New strategies are needed.
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PMID:MS Forum/MS Over the Past 17 Years. 2168 89

Relapse is a highly prevalent phenomenon in addiction. This paper examines the new research on identifying biological factors that contribute to addiction relapse risk. Prospective studies examining relapse risk are reviewed, and clinical, biological, and neural factors that predict relapse risk are identified. Clinical factors, patient-related factors, and subjective and behavioral measures such as depressive symptoms, stress, and drug craving all predict future relapse risk. Among biological measures, endocrine measures such as cortisol and cortisol/corticotropin (ACTH) ratio as a measure of adrenal sensitivity and serum brain-derived neurotrophic factor were also predictive of future relapse risk. Among neural measures, brain atrophy in the medial frontal regions and hyperreactivity of the anterior cingulate during withdrawal were identified as important in drug withdrawal and relapse risk. Caveats pertaining to specific drug abuse type and phase of addiction are discussed. Finally, significant implications of these findings for clinical practice are presented, with a specific focus on determining biological markers of relapse risk that may be used to identify those individuals who are most at risk of relapse in the clinic. Such markers may then be used to assess treatment response and develop specific treatments that will normalize these neural and biological sequelae so as to significantly improve relapse outcomes.
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PMID:New findings on biological factors predicting addiction relapse vulnerability. 2179 80