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)

It is currently believed that Parkinson disease (PD) is due to a degenerative process that independently damages multiple areas of the central and peripheral nervous system. Loss of nigrostriatal dopamine is now widely recognized as being directly related to the motor symptoms in Parkinson's disease. Parkinsonian patients also exhibit symptoms and signs suggestive of hypothalamic dysfunction (e.g. dysautonomia, impaired heat tolerance). The latter clinical features are supported by pathological, biochemical and endocrinological findings. Lewy body formation has been demonstrated in every nucleus of the hypothalamus, specifically the tuberomamillary and posterior hypothalamic. Preferential involvement of the hypothalamus was also noted in patients after post-encephalitic parkinsonism. Loss of dopamine (30-40%) in the hypothalamus of affected patients has been shown in recent studies, and is compatible with the reported abnormalities of growth hormone release in response to L-dopa administration, elevated plasma levels of MSH, and reduced CSF levels of somatostatin and beta-endorphins in these patients. Deranged immunological mechanisms have been found in PD patients including the presence of autoantibodies against sympathetic ganglia neurons, adrenal medulla and caudate nucleus. On the evidence of on pathological studies demonstrating the early vulnerability of the hypothalamus in aging and PD, and the known role of the hypothalamus in immune modulation, we expect that it will be shown that primary damage of the hypothalamus leads to subsequent secondary degeneration of structures receiving direct projections from the hypothalamus. Within this framework, the dopaminergic systems may be damaged, since striatal dopamine synthesis and receptor sensitivity have been shown to be regulated by ACTH and alpha-MSH through direct arcuate nucleus-striatal projections.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The hypothalamus in Parkinson disease. 288 37

The present study was aimed at investigating the relationship between "chronic constitutional tetany" (spasmophilia) and headache. Several adult patients presenting with neuromuscular hyperexcitability, anxiety, dysautonomia, and oculofrontal headache were subjected to a series of ion and hormone blood tests, and the results were compared with those in control subjects. Calcium and parathyroid hormone levels were significantly decreased, and phosphorus and beta-endorphin-like immunoreactivity were significantly increased. A subgroup of the patients had all four abnormalities. In most cases the family history was positive for headache. Sleep disturbances and personal histories of periodic syndrome in infancy were recorded. It is concluded that a correlation may exist between the symptoms assessed and an impairment of some ion and hormone levels. There are several traits in common with "common migraine", and our patients may form a subgroup of that group. A possible linkage between headache/tetany and the periodic and hyperventilation syndromes is discussed. The increased beta-endorphin-like immunoreactivity is putatively a reactive phenomenon.
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PMID:Calcium deficiency and supraorbital headache: a clinical study of adult subjects. 294 51

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.
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PMID:Intermittent hypoendorphinaemia in migraine attack. 629 72

Fatal familial insomnia is a prion disease in which a selective thalamic degeneration leads to total sleep deprivation, hypertension, dysautonomia, adrenal overactivity, and impaired motor functions. With patients under continuous recumbency and polysomnographic control, we assessed the changes in the 24-hour patterns of blood pressure, heart rate, plasma catecholamines, corticotropin, and serum cortisol in three patients at different stages of the disease. Six healthy volunteers were used as control subjects. A dominant 24-hour component was detected at rhythm analysis of all variables, both in patients and control subjects. In the patients, the amplitudes gradually decreased as the disease progressed, leading to the obliteration of any significant dirunal variation only in the preterminal stage. A shift in phase corresponded to the loss of the nocturnal fall in blood pressure in an early stage of the disease, when nocturnal bradycardia was still preserved. Plasma cortisol was high and became increasingly elevated, whereas corticotropin remained within normal levels; abnormal nocturnal peaks appeared in their circadian patterns. The disrupted patterns of cortisol and blood pressure preceded the development of hypertension and severe dysautonomia, which in turn were paralleled by increasing catecholamine and heart rate levels. Our data demonstrate that in patients with fatal familial insomnia the changes detectable in the rhythmic component of diurnal blood pressure variability result in a pattern of secondary hypertension. Disturbances in thalamic, pituitary-adrenal, and autonomic functions seem to be involved in mediating these changes.
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PMID:Diurnal blood pressure variation and hormonal correlates in fatal familial insomnia. 817 63