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 neuropeptides vasopressin, adrenocorticotropin (ACTH), and beta-endorphin seem to have important effects on memory and learning. Animal studies attempting to demonstrate these effects are difficult to interpret because of the complexity of behavior that is described as "learning" and the impossibility of assessing verbal learning in animals. This article therefore reviews some of the animal literature on neuropeptides and learning, but focuses primarily upon studies in humans, both in normal volunteers and in patients with neurological disorders. Vasopressin enhances learning under some conditions. Intranasal administration has been associated with improvement on psychometric tests in patients with mild Alzheimer's disease and Korsakoff's psychosis, although these findings are not uniform. It improves performance on memory tests in normal volunteers, but does not seem to improve the memory deficit after head trauma. Cerebrospinal fluid levels are low in patients with Alzheimer's disease. ACTH and melanocyte-stimulating hormone (MSH) are two peptides the primary behavioral effect of which seems to be on attention or goal-motivated behavior rather than on memory processes themselves. Visual discrimination and the ability to continue repetitive tasks are enhanced; in mentally retarded subjects, the administration of ACTH or MSH improves performance on a variety of neuropsychological tests. It does not, however, improve cognitive function in the elderly. Endogenous opioids including beta-endorphin and met-enkephalin seem to have primarily an amnesic effect in animal studies. Their role in human learning is still uncertain, although naloxone, which antagonizes their effects, has been associated with improved cognitive performance in patients with Alzheimer's disease. These data underscore the complexity of the processes associated with human memory and the rudimentary state of our present knowledge. Whatever the mechanisms, however, vasopressin, ACTH, and endogenous opioids seem to have important effects upon memory.
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PMID:Neuropeptides in human memory and learning processes. 299 44

We examined corticotropin-releasing hormone-like immunoreactivity (CRH-LI) and corticotropin (ACTH) levels in the CSF of 33 patients with presumptive Alzheimer's disease (AD) and 13 healthy, age-matched controls. The mean CRH-LI and ACTH levels of the AD patients were significantly less than controls. Despite these reductions, none of the patients had evidence of pituitary-adrenal dysfunction. A disorder of extrahypothalamic CRH may be involved in the pathophysiology of AD.
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PMID:Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH) and corticotropin (ACTH) are reduced in patients with Alzheimer's disease. 302 28

We measured CSF levels of the opioid peptides beta-endorphin and beta-lipotropin in patients with Alzheimer's disease, multi-infarct dementia and controls. In both dementia groups, the mean concentration of beta-endorphin was significantly lower than in controls. The mean beta-lipotropin levels did not differ significantly in the two groups. The low CSF beta-endorphin level may relate generally to dementia.
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PMID:CSF beta-endorphin and beta-lipotropin in Alzheimer's disease and multi-infarct dementia. 315 72

Using a sensitive double-antibody solid-phase enzyme immunoassay method alpha-melanocyte stimulating hormone-like immunoreactivity (alpha-MSH-LI) was measured in 21 regions of postmortem brains from 8 normal subjects and 5 patients with Alzheimer-type dementia (ATD). In the brains from the normal subjects, the highest concentration of alpha-MSH-LI was found in the hypothalamus. Relatively high concentration were also measured in the locus coeruleus, substantia innominata, substantia nigra, amygdala and medial nucleus of thalamus. alpha-MSH-LI in other regions was approximately 1/100 of the hypothalamic content. This data is consistent with the existence of alpha-MSH in extrahypophyseal regions and indicates its regional distribution in the human brain. In the Alzheimer brains, although the temporal cortex and hippocampus had normal concentrations of alpha-MSH-LI, the cingulate cortex, caudate and substantia nigra showed significantly lower concentrations of alpha-MSH-LI than those of the control brains. This data suggests that further studies of alpha-MSH content in a larger number of ATD brains would be useful.
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PMID:Extrahypophyseal distribution of alpha-melanocyte stimulating hormone (alpha-MSH)-like immunoreactivity in postmortem brains from normal subjects and Alzheimer-type dementia patients. 352 51

The hypothesis is that a functional deficiency of alpha-melanotropin (alpha-MSH) is the primary event in the development of Alzheimer's disease. Beginning with the concept that Alzheimer's disease occurs because of a deficiency of a neurotrophic factor specific for central cholinergic neurons data is then presented to support the hypothesis that alpha-MSH is the critical neurotrophic factor.
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PMID:Is alpha-MSH deficiency the cause of Alzheimer's disease? 363 64

Several authors have reported reduced levels of pro-opiomelanocortin (POMC)-related peptides in the cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), but the mechanisms regulating the CSF content of these substances are still debated. In this case report the processing of POMC peptides has been investigated post-mortem (HPLC and RIA methods) at the pituitary and hypothalamic level in an AD patient and in a control subject. From the results obtained it seems likely that defects of axonal transport and/or secretion rather than synthesis could account for the abnormalities of POMC peptides in the CSF.
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PMID:Abnormal pro-opiomelanocortin processing in Alzheimer's disease. A case report. 369 76

Cerebrospinal fluid (CSF) concentrations of ACTH, beta-lipotropin (beta-LPH) and beta-endorphin (beta-EP) were measured in 15 patients affected by dementia, who underwent also a brain computerized tomography (CT), and in 13 age-matched healthy volunteers. ACTH CSF levels of patients (4.0 +/- 2.4 fmol/ml, M +/- SD) were significantly lower than in controls (9.8 +/- 5.0, P less than 0.01) the lowest values being found in Alzheimer type of dementia (ATD: 3.1 +/- 2.5) and in patients with radiological evidence of cortical atrophy (2.5 +/- 1.2), independently of the probable origin of dementia. Although beta-LPH and beta-EP levels of patients fell within normal range, they were lower in ATD than in dementia sustained on a vascular origin. There was no variation of either peptides concentration in relation to CT findings. These data indicate the ACTH impairment as typical of dementia, supporting in humans the positive role of this peptide on learning and mnesic functions. Moreover, the maintained CSF levels of both beta-LPH and beta-EP in the dementia sustained on a vascular origin, while lower values were found in ATD, could represent a differentiation between vascular and degenerative diseases of the Central Nervous System (CNS).
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PMID:Central ACTH deficit in degenerative and vascular dementia. 609 Aug 45

The primary lesion in Alzheimer's disease and dialysis dementia has been postulated to be an impaired blood-brain-barrier (BBB) permeability that allows neurotoxins like aluminium to reach the central nervous system. The present study shows that aluminium itself affects the permeability of the BBB of rats to small peptides. Intraperitoneal injection of aluminium chloride increased the permeability of the BBB to iodinated N-Tyr-delta-sleep-inducing peptide and beta-endorphin by 60-70%. Thus, aluminium can affect the BBB in ways that might be involved in dementia.
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PMID:Aluminium increases permeability of the blood-brain barrier to labelled DSIP and beta-endorphin: possible implications for senile and dialysis dementia. 613 73

Neuropeptides are sufficiently stable to allow valid radioimmunoassay of peptide concentrations in post-mortem human nervous tissue and in human cerebrospinal fluid. Studies have now documented abnormalities of peptide concentrations in degenerative diseases of the brain. Somatostatin concentration is reduced in the hippocampus and neocortex of patients dying with Alzheimer's type dementia. In Huntington's disease, there are reduced concentrations of substance P, met-enkephalin and cholecystokinin in the basal ganglia; in contrast the concentrations of somatostatin and TRH are increased. Immunocytochemical and experimental lesion studies are underway in an attempt to localize the peptide-containing cells affected by these disorders; and the potential role of alterations in neuropeptide function in the pathogenesis, clinical manifestations and therapy of these illnesses is of great interest. Although alterations of CSF peptide concentrations have been reported in a variety of human diseases, interpretation of these results requires knowledge of the origin and disposition of CSF peptides. Future research into the pathology of peptidergic systems will depend on the development of specific peptide antagonists to probe dynamic aspects of peptide function and on the application of the tools of molecular biology, such as specific mRNA assays, to human material.
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PMID:Implications of neuropeptides in neurological diseases. 620 11

Levels of corticotropin-releasing hormone (CRH) in cerebrospinal fluid (CSF) were examined in patients with spinocerebellar degeneration (SCD) including olivopontocerebellar atrophy (OPCA), dentatorubropallidoluysian atrophy (DRPLA) and Friedreich's ataxia, Parkinson's disease (PD) and senile dementia of the Alzheimer type (SDAT), and normal aged subjects. CRH concentrations in CSF were significantly reduced in SCD compared to SDAT, PD and CSF and normal aged subjects. It is likely that degeneration not only of the cerebral cortex and the limbic system but also of the subcortical structures such as the brainstem and the cerebellum alters levels of CRH in CSF. Together with the recent anatomical and physiological evidence, the results suggest pathophysiological relevance of CRH for the cerebellar symptoms in SCD.
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PMID:Cerebrospinal fluid corticotropin-releasing hormone in neurodegenerative diseases: reduction in spinocerebellar degeneration. 747 76


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