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)

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
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PMID:Somatostatin in Alzheimer's disease and depression. 135 21

In 38 old aged parkinsonian patients, two major subgroups could be established: one with predominant akinesia, rigidity, postural instability and accompanying cognitive impairment with intellectual deterioration correlated with duration of disease but not with age of onset and another with predominant tremor and relatively intact intellectual functions. The mean somatostatin-like immunoreactivity (SLI) level in the cerebrospinal fluid (CSF) was significantly lower in parkinsonian patients (21.4 +/- 8.1 fmol ml-1) compared to senile control patients (29.5 +/- 9.4 fmol ml-1). In contrast to senile dementia of Alzheimer's type SLI was not correlated with dementia scores but with motor disease progression. Homovanillic acid (HVA) significantly decreased only in patients without L-DOPA treatment. Correlations between SLI, HVA and 5-hydroxyindole acetic acid (5-HIAA) indicate a degeneration of multiple neuronal networks which includes somatostatinergic neurons.
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PMID:Parkinson's disease and dementia: clinical and neurochemical correlations. 137 66

Cerebrospinal fluid concentrations of corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) were measured in 77 female inpatients with moderate to extreme dementia and in 17 elderly female controls. Both multi-infarct (MID) and Alzheimer-type (SDAT) demented patients had equally elevated CSF CRH and TRH but not SRIF levels as compared with the controls. This elevation was, however, not seen in patients with simple dementia while it was most prominent in those exhibiting marked depressive symptoms. It is concluded that depression rather than dementia itself may be associated with CSF CRH and TRH elevation in elderly patients with cognitive impairment.
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PMID:Cerebrospinal fluid neuropeptides in dementia. 148 50

Extensive electrical stimulation of the perforant pathway input to the hippocampus results in a characteristic pattern of neuronal death, which is accompanied by an impairment of cognitive functions similar to that seen in human temporal lobe epilepsy. The excitotoxic hypothesis of epileptic cell death [Olney, J. W. (1978) in Kainic Acid as a Tool in Neurobiology, eds. McGeer, E., Olney, J. W. & McGeer, P. (Raven, New York), pp. 95-121; Olney, J. W. (1983) in Excitotoxins, eds. Fuxe, K., Roberts, P. J. & Schwartch, R. (Wenner-Gren International Symposium Series, Macmillan, London), Vol. 39, pp. 82-96; and Rothman, S. M. & Olney, J. W. (1986) Ann. Neurol. 19, 105-111] predicts an imbalance between excitation and inhibition, which occurs probably as a result of hyperactivity in afferent pathways or impaired inhibition. In the present study, we investigated whether the enhancement of gamma-aminobutyric acid (GABA)-mediated (GABAergic) inhibition of neurotransmission by blocking the GABA-metabolizing enzyme, GABA transaminase, could influence the histopathological and/or the behavioral outcome in this epilepsy model. We demonstrate that the loss of pyramidal cells and hilar somatostatin-containing neurons can be abolished by enhancing the level of synaptically released GABA, and that the preservation of hippocampal structure is accompanied by a significant sparing of spatial memory as compared with placebo-treated controls. These results suggest that enhanced GABAergic inhibition can effectively block the pathophysiological processes that lead to excitotoxic cell death and, as a result, protect the brain from seizure-induced cognitive impairment.
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PMID:Enhanced GABAergic inhibition preserves hippocampal structure and function in a model of epilepsy. 165 57

Reduced brain and cerebrospinal fluid (CSF) levels of somatostatin, corticotropin-releasing hormone (CRH) and corticotropin (ACTH) have been reported among neuropsychiatric patients with cognitive dysfunction. Alcoholism is a disorder in which associated neuropsychiatric disorders occur. Therefore, we compared CSF levels of somatostatin, CRH and ACTH in alcoholics (n = 100) and normal controls (n = 30). There were no significant differences between the groups in concentrations of the 3 peptides. Moreover, there were no significant correlations between concentrations of the peptides in CSF and computed tomographic measures of the size of brain ventricles. There were, however, significant correlations between CSF concentrations of CRH and ACTH and between CSF concentrations of CRH and somatostatin in both the alcoholic and control groups.
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PMID:Cerebrospinal fluid levels of somatostatin, corticotropin-releasing hormone and corticotropin in alcoholism. 197 69

The level of cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 11 chronic schizophrenic patients with moderate cognitive impairment and for 8 controls. The CSF SLI was significantly reduced (37%) in schizophrenic patients, but this decrease did not correlate with the degree of cognitive decline measured by the Mini-Mental State Examination, with psychotic symptoms estimated by the Brief Psychiatric Rating Scale, or with the neuroleptic dose. Although a reducing effect of long-term neuroleptic treatment cannot be totally excluded, the present study suggests that the CSF SLI level is decreased in cognitively impaired schizophrenic patients, as in many other disorders with cognitive impairment.
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PMID:Decreased somatostatin-like immunoreactivity in the cerebrospinal fluid of chronic schizophrenic patients with cognitive impairment. 224 5

Cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 9 patients with chronic alcohol ingestion and dementia associated with alcoholism and for 8 age-equivalent controls. The CSF SLI was significantly reduced (32%) in the alcoholics with dementia as compared to the controls. This finding is in accordance with previous observations on the relationship between reduced CSF SLI and cognitive impairment in various neuropsychiatric disorders, and extends this finding to patients with dementia associated with alcoholism.
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PMID:Somatostatin-like immunoreactivity in the CSF of patients with dementia associated with alcoholism. 228 44

Huntington's disease (HD) is an autosomal dominant neurological disorder characterized by progressive chorea, cognitive impairment and emotional disturbance. The disease usually occurs in midlife and symptoms progress inexorably to mental and physical incapacitation. It has been postulated that an excitotoxin is involved in the pathogenesis of HD. Schwarcz and colleagues have shown that quinolinic acid (QA) can produce axon-sparing lesions similar to those observed in HD. The lesions result in a depletion of neurotransmitters contained within striatal spiny neurones, for example gamma-aminobutyric acid (GABA), while dopamine is unaffected. Recently, we and others have demonstrated that in HD striatum there is a paradoxical 3-5-fold increase in both somatostatin and neuropeptide Y which is attributable to selective preservation of a subclass of striatal aspiny neurones in which these peptides are co-localized. In the present study we demonstrate that lesions due to quinolinic acid closely resemble those of HD as they result in marked depletions of both GABA and substance P, with selective sparing of somatostatin/neuropeptide Y neurones. Lesions produced by kainic acid (KA), ibotenic acid (IA) and N-methyl-D-aspartate (MeAsp) were unlike those produced by QA, as they affected all cell types without sparing somatostatin/neuropeptide Y neurones. These results suggest that QA or a similar compound could be responsible for neuronal degeneration in HD.
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PMID:Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid. 242 61

Cerebrospinal fluid somatostatin-like immunoreactivity (CSF SLI) was determined for 67 elderly patients who met the DSM-III criteria for delirium and for 19 age-matched controls. As a group, and also when subdivided according to the type of delirium, severity of cognitive decline or the type of central nervous system disease, the delirious patients showed significant reductions of SLI compared with the controls, together with a declining trend associated with increasing cognitive dysfunction. These findings are in accordance with previous observations that reduced CSF SLI is associated with diseases in which cognitive function is disturbed and they extend this finding to delirium.
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PMID:Cerebrospinal fluid somatostatin in delirium. 257 25

A nonfamilial syndrome is described in two middle-aged men who presented with progressive aphasia without incipient signs of cognitive impairment. In each case, 2 years elapsed before progressive functional decline or behavioral disabilities supervened. Radiologic studies documented asymmetric left cerebral atrophy that was progressive. The structure of the language disintegration was distinctive and not like that in Alzheimer's disease. Pathologic studies performed at postmortem examination of one patient documented asymmetric cerebral atrophy with nonspecific histopathologic changes. Biochemical studies revealed normal tissue levels of choline acetyltransferase activity, but reduced somatostatin-like immunoreactivity. Since cerebral somatostatin is largely present in intrinsic cortical neurons, while cholinergic innervation is largely derived from the basal forebrain, these findings suggest that nonfamilial dysphasic dementia may be an example of a distinct class of dementia due to intrinsic cortical degeneration, with sparing of the basal forebrain.
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PMID:Reduced somatostatin-like immunoreactivity in cerebral cortex in nonfamilial dysphasic dementia. 288 51


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