Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antisera to neuropeptide Y (NPY) gave an intense immunohistochemical reaction of certain nerve cells in the myenteric and submucous plexuses of the guinea-pig small intestine. Each nerve cell had up to 20 branching, tapering processes that were less than approximately 50 micron long and a long process that could be followed for a considerable distance. This morphology corresponds to that of the type-III cells of Dogiel. The long process of each myenteric cell ran through the circular muscle to the submucosa, and in most cases the process could be traced to the mucosa. The submucous nerve cell bodies also had processes that extended to the mucosa. These cell bodies, in both plexuses, also stained with antisera raised against calcitonin gene-related peptide (CGRP), cholecystokinin (CCK), choline acetyltransferase (ChAT) and somatostatin (SOM), but did not stain with antibodies against enkephalin, substance P or vasoactive intestinal peptide. Thus, it has been possible for the first time to trace the processes of chemically specified neurons through the layers of the intestinal wall and to show by a direct method that CGRP/CCK/ChAT/NPY/SOM myenteric and submucous nerves cells provide terminals in the mucosa.
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PMID:Neurochemically similar myenteric and submucous neurons directly traced to the mucosa of the small intestine. 383 15

Both Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) are progressive dementias characterized neuropathologically by the presence in the cerebral cortex of numerous neurofibrillary tangles and neuritic plaques. We use the abbreviation AD/SDAT to denote all such cases, irrespective of age of onset. Studies of neurotransmitter-related parameters in autopsied brain tissues from patients with AD/SDAT have, to date, been confined to five putative transmitter systems. Acetycholine-releasing neurones seem to be most markedly and consistently affected, as judged by the extensive reductions in choline acetyltransferase (ChAT) and acetylcholinesterase activities that have been reported. Despite numerous studies, there is no consistent evidence for the involvement of neurones releasing dopamine, noradrenaline, serotonin, or gamma-aminobutyric acid in AD/SDAT, nor for loss of muscarinic cholinergic receptors. Thus, the involvement of cholinergic neurones in AD/SDAT seems to be specific. However, the possible involvement of neurones using other chemicals as transmitters has yet to be explored. The recent recognition of the existence of so-called 'peptidergic neurones' in the mammalian brain (for review see ref. 8) and the availability of radioimmunoassay (RIA) techniques for studying these peptides, have led us to begin a systematic investigation of neuropeptides in autopsied brain tissue from cases of AD/SDAT, and from neurologically normal individuals. We report here results obtained with a RIA for somatostatin, showing that somatostatin-like immunoreactivity in the cerebral cortex is reduced in tissue from AD/SDAT patients.
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PMID:Reduced somatostatin-like immunoreactivity in cerebral cortex from cases of Alzheimer disease and Alzheimer senile dementa. 610 62

Post-mortem brain tissue from 15 patients dying with a diagnosis of senile dementia of Alzheimer type (SDAT) was compared with tissue obtained from 16 control patients at routine post-mortem. A significant fall in choline acetyltransferase (ChAT) activity was observed in the cortex, hippocampus and amygdala of the SDAT cases and was maximal in the temporal cortex. The fall in ChAT activity observed in the temporal cortex was accompanied by a significant reduction (47%) in immunoreactive somatostatin.
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PMID:Reduced amounts of immunoreactive somatostatin in the temporal cortex in senile dementia of Alzheimer type. 610 40

The activity of choline acetyltransferase (ChAT) and the concentration of somatostatin-like immunoreactive material (SLI) have been measured in 8 brain regions from 12 normal individuals and 12 cases of presenile and senile dementia of the Alzheimer type. ChAT activity was significantly lower in all 8 brain regions of demented patients and the SLI concentration was significantly reduced in 7 of the the 8. There were correlations between the extent of the reductions of ChAT activity and SLI concentration in four brain regions, and a greater reduction of parietal cortex SLI in younger patients than in the more elderly.
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PMID:Cortical somatostatin-like immunoreactivity in cases of Alzheimer's disease and senile dementia of the Alzheimer type. 611 27

The somatostatin content and choline acetyltransferase activity of the rat cerebral cortex and hippocampus were examined after lesions to the nucleus basalis, the fornix and the dorsal hippocampus. Lesions of the nucleus basalis caused reductions in cortical choline acetyltransferase activity but had no effect on the concentration of somatostatin. Fornix transection caused a reduction in choline acetyltransferase activity in the dorsal hippocampus, but again was without effect on the somatostatin content. Excitotoxin lesions of the dorsal hippocampus caused a 69% reduction in somatostatin concentration in this structure, with no reduction in choline acetyltransferase activity. The results indicate that somatostatin and choline acetyltransferase are in separate populations of neurons in the rat cerebral cortex and hippocampus.
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PMID:Somatostatin is not co-localized in cholinergic neurons innervating the rat cerebral cortex-hippocampal formation. 612 55

Dementia of the Alzheimer type (DTA) is the most common form of adult-onset dementia. The clinical features of the disease include progressive memory defect, intellectual impairment and behavioral disturbances. The number of patients suffering from DTA is increasing dramatically, due to the growing proportion of old people. DTA therefore is a major public health problem. Brain lesions include several histopathological changes (mostly in the cerebral cortex and hippocampus): neurofibrillary tangles, senile plaques, granulo-vacuolar degeneration, Hirano bodies, angiopathy, loss of nerve cells. Postmortem brain examination reveals characteristic neurochemical deficits. The most consistent reduction in neurotransmitter-synthesizing enzyme observed so far is a reduction in choline acetyltransferase activity, suggesting a cholinergic deficit. However, other deficits involving noradrenaline and somatostatin have also been reported. Several hypotheses (genetic, viral, toxic, immunologic, metabolic) have been put forward in order to explain DTA. The relationship between these hypotheses and the neurochemical deficits is still unclear, but the existence of characteristic neurotransmitter-related deficits allows specific therapeutic trials.
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PMID:[Alzheimer's type dementia: recent data]. 613 79

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75

Concentrations of somatostatin-like immunoreactivity (SRIF-LI) were measured in cerebral cortex, hippocampus, septum-POA, median eminence, gastric antrum, fundus and pancreas in adult female hamsters to determine whether changes in somatostatin could be related to increased growth hormone (GH) secretion and somatic growth that follow bilateral transections of hippocampus (n = 18; 17 controls). In addition, choline acetyltransferase (CAT) activity was measured in the four brain regions in hippocampectomized (n = 10) and control hamsters (n = 10) to gain insight into the relationship between these two neurotransmitters. Hippocampal transections induced: significant acceleration of somatic growth; increased serum GH concentrations; increased concentrations of SRIF-LI in septum-POA and gastric antrum; reduced concentrations of SRIF-LI in hippocampus and pancreas; and reduced CAT activity in the hippocampus. These results suggest that somatostatinergic and cholinergic projections to hippocampus via fornix suppress GH and somatic growth in adult hamsters and that reduced release of SRIF-LI in the gastric antrum may contribute to the acceleration of somatic growth through facilitated nutrient digestion and entry.
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PMID:A role for somatostatin in the control of hamster growth. 614 Sep 95

Assessment of neurochemical markers in the frontal cortex indicates that choline acetyltransferase is significantly decreased in Alzheimer's and Gerstmann-Straussler dementias but not in Pick's dementia. It therefore appears that the cholinergic innervation of the cortex from the basal forebrain is intact in Pick's disease. Cortical somatostatin was decreased only in Alzheimer's disease (AD), indicating that loss of somatostatin is not a constant feature in different forms of dementia. Muscarinic binding sites were unaltered in Pick's disease and Gerstmann-Straussler syndrome but were decreased in a subpopulation of AD patients. These data suggest that in some cases of AD a significant loss of cholinoceptive neurones in the cortex is evident.
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PMID:A post-mortem comparison of the cortical cholinergic system in Alzheimer's disease and Pick's disease. 614 96

Brains of 49 patients who had died with Alzheimer's disease and 54 controls were examined. The Alzheimer group exhibited noticeably reduced activity of the cholinergic marker enzyme choline acetyltransferase in the cerebral cortex, but cortical concentrations of noradrenaline, gamma-aminobutyric acid, and somatostatin were also significantly reduced. Analysis of the results according to age at death showed that the older patients, dying in their 9th and 10th decades, had a relatively pure cholinergic deficit confined to temporal lobe and hippocampus, together with a reduced concentration of somatostatin confined to temporal cortex. By contrast, the younger patients, dying in their 7th and 8th decades, had a widespread and severe cholinergic deficit together with the abnormalities of noradrenaline, gamma-aminobutyric acid, and somatostatin, and the younger patients accounted for most of the abnormalities in these systems observed in the overall group. Comparison of the young subjects with Alzheimer's disease with the older controls did not support the concept of Alzheimer's disease representing an acceleration of the aging process. These results suggest that Alzheimer's disease in people aged under 80 may represent a distinct form of presenile dementia which differs in important respects from the dementia of old age.
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PMID:Neurochemical characteristics of early and late onset types of Alzheimer's disease. 614 50


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