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)

The concentration of the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA), was measured in the cerebral cortex obtained at diagnostic craniotomy from 10 patients with Alzheimer's disease of 3 yrs mean duration and 6 patients with other causes of dementia, and from 31 subjects undergoing other neurosurgical procedures (for which removal of apparently normal tissue was necessary). GABA content of 5 areas of the cerebral cortex and the cerebellar cortex was measured postmortem in the brains of 23 Alzheimer and 19 control subjects and 5 patients with other causes of dementia. Fourteen of these specimens, including 7 from patients with Alzheimer's disease of 8 yrs mean duration, were obtained within 3 h of death. These were processed in a similar manner to the neurosurgical specimens and are regarded also as fresh tissue samples. The remaining 33 specimens are regarded as conventional postmortem samples as the mean interval of death to autopsy was 21 h. GABA concentration in conventional autopsy specimens from Alzheimer subjects was not reduced as compared with controls in either cingulate or cerebellar cortex. In the inferior parietal cortex, agonal status confounded this comparison. The concentration was reduced in superior parietal, frontal and temporal cortex but there is a possibility that agonal state also confounded these comparisons. There was no deficit in GABA concentration in fresh cortical tissue from Alzheimer patients except for the temporal lobe from autopsy specimens. The content of somatostatin-like immunoreactivity was, like GABA, found to be comparable to control in some groups of Alzheimer specimens. It is argued that the deficits in autopsy samples and lack of change in surgical specimens is likely to be due to the duration of illness at the time of sampling. Losses of choline acetyltransferase activity were observed in all groups of Alzheimer specimens in all areas of brain studied. The data are consistent with other results which suggest that cholinergic under-activity is most closely related to the clinical course of Alzheimer's disease.
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PMID:Gamma-aminobutyric acid concentration in brain tissue at two stages of Alzheimer's disease. 340 83

Post-mortem pathological and biochemical studies are reported on six patients with progressive dementia. The characteristic pathological finding was neurofilament-containing cytoplasmic inclusions in cortical and subcortical neurons. The clinical and pathological findings were consistent with so-called diffuse Lewy body disease. The patients had variable changes of the Alzheimer type, with five of six patients displaying "plaques only" Alzheimer's changes. Biochemical studies showed profound decreases in neocortical choline acetyltransferase (ChAT) activities that correlated with marked neuronal loss in the basal nucleus of Meynert. ChAT activities were normal in the hippocampus in three patients who also had no significant Alzheimer type hippocampal changes. All patients had decreased cortical somatostatin-like immunoreactivity. Our observations suggest that dementia in diffuse Lewy body disease bears biochemical similarities to Alzheimer's disease, in that biochemical markers for both intrinsic cortical neurons and ascending cholinergic neurons are affected.
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PMID:Diffuse Lewy body disease. Neuropathological and biochemical studies of six patients. 343 18

Somatostatin-like immunoreactivity (SLI) and acetylcholinesterase (AchE) activities were measured in the cerebrospinal fluid of 25 patients with senile dementia of the Alzheimer type (SDAT). Both SLI levels and AchE activities were reduced in the CSF of SDAT patients. The SLI levels and AchE activities were not correlated with the duration and the dementia score. However, in two patients the CSF SLI concentration was in agreement with the SLI levels in the frontal cortex obtained by biopsy. Our findings suggest that CSF SLI may be a good index of cortical SLI activities.
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PMID:Somatostatin-like immunoreactivity and acetylcholinesterase activities in cerebrospinal fluid of patients with Alzheimer disease and senile dementia of the Alzheimer type. 351 22

A systematic endocrine investigation in dementia, depression and control subjects showed that plasma growth hormone (GH) was higher in the morning and plasma TSH concentrations were higher throughout the day in Alzheimer-type dementia (ATD) than in age-matched depressed patients (MDD), and plasma TSH concentrations were also higher throughout the day in female ATD compared with age-matched female control subjects. The increased plasma TSH concentrations could not be due to reduced negative feedback because plasma T3, T4 and rT3 were in the normal range. Plasma concentrations of oestrogen-stimulated neurophysin (ESN) were lower throughout the day in ATD compared with MDD and controls and lower in the morning compared with other dementias. The high plasma GH and TSH concentrations in ATD may reflect the reduced hypothalamic content of somatostatin in ATD, and the reduced concentrations of ESN may reflect reduced cholinergic activity in ATD brain. These selective hormonal changes provide a useful diagnostic test for Alzheimer's disease.
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PMID:Characteristic plasma hormone changes in Alzheimer's disease. 365 5

Somatostatin-like immunoreactivity (SLI) was measured in postmortem brain tissue from 15 control patients, 7 non-demented parkinsonian patients and 7 demented parkinsonian patients who had Alzheimer-type cortical pathology. The non-demented parkinsonian patients had normal concentrations of SLI in the cerebral cortex, hippocampus, amygdala, putamen, caudate or globus pallidus. Demented parkinsonian patients with Alzheimer-type cortical pathology had significantly reduced (approximately 40%) levels of SLI in both the frontal (Brodmann area 6) and temporal (Brodmann area 21) cortex. These findings suggest that parkinsonian dementia with Alzheimer-type pathology like Alzheimer's disease itself, is associated with reduced concentrations of cortical somatostatin.
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PMID:Somatostatin immunoreactivity is reduced in Parkinson's disease dementia with Alzheimer's changes. 380 78

To investigate changes in the somatostatinergic neurons of patients with Alzheimer's disease (AD), we determined the somatostatin-like immunoreactivity (SLI) in post-mortem brain tissue of histopathologically confirmed AD patients and in CSF of probable AD patients (according to DSM III). The CSF values were then correlated with psychological test scores. In 6 AD patients the SLI values were decreased 42% (P less than 0.005) in the frontal cortex, 28% (P less than 0.05) in the temporal cortex and 42% (P less than 0.01) in the parietal cortex but not in the thalamus and putamen compared to 11 control patients. In some brain areas there were statistical correlations between SLI values and cholinergic markers, choline acetyltransferase and acetylcholine esterase activities, suggesting a relationship between these two neurotransmitter systems. In the CSF among 75 AD patients SLI was 35% lower (P less than 0.001) than in controls. Severely demented power (P less than 0.001) than in controls. Severely demented patients showed lower SLI values than moderately demented individuals, but this difference was not significant. There was a weak but statistically significant correlation between SLI values in CSF and neuropsychological test scores. This study further confirms the involvement of somatostatinergic neurons in AD and suggests that this involvement may be related to the progression of dementia symptoms.
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PMID:Decreased somatostatin-like immunoreactivity in cerebral cortex and cerebrospinal fluid in Alzheimer's disease. 382 77

Parkinson's disease is characterized by a deficiency of dopamine in the nigrostriatal system. However, changes in dopamine neurons were found also outside the extrapyramidal system, showing that there is a more general brain defect than just the loss of substantia nigra dopamine neurons. With regard to the behavior of striatal D-2 receptors it was possible to divide parkinsonian patients into two subgroups, because either a decrease or an increase in the number of D-2 receptors was found. Clinically, the patients with a decreased number of striatal D-2 receptors were more disabled and had lost the beneficial response to levodopa. D-3 receptor binding sites were decreased in the parkinsonian striatum. Changes in the cholinergic-muscarinic receptors in the striatum seem to be related to changes in D-2 receptors, and muscarinic receptor supersensitivity was found in cortical areas. GABA receptor binding was decreased in the substantia nigra. In the parkinsonian brain there seems to be supersensitivity of a population of enkephalin receptors (delta) in the striatum and in the limbic system and also a loss of others (mu) in the striatum. Furthermore, the Met-enkephalin content was decreased in the parkinsonian substantia nigra. A decreased concentration of substance P was found in the substantia nigra of all parkinsonian patients and in the putamen of those patients who had not received levodopa treatment. The somatostatin level was decreased in the frontal cortex in relation to dementia. There are thus multiple neuronal disturbances in the parkinsonian brain, although those of the nigrostriatal dopamine neurons seem to be the greatest and are more closely related to parkinsonian clinical features and to treatment responses.
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PMID:Brain neurotransmitters and neuropeptides in Parkinson's disease. 609 88

Thyrotrophin-releasing hormone and gonadotrophin-releasing hormone were measured in lumbar CSF from patients with idiopathic senile dementia, cerebral tumours and spinal disc lesions. Somatostatin was also measured in lumbar CSF from patients with dementia and patients with other neurological disorders, but the numbers involved were much smaller. The levels of these neuropeptides were significantly reduced in the patients with senile dementia. These results suggest a possible involvement of hpothalamic neuropeptides in idiopathic senile dementia.
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PMID:Investigation of cerebrospinal fluid neuropeptides in idiopathic senile dementia. 611 46

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


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