Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Somatostatin displays a regulatory function on several aminergic neurotransmitters, including dopamine. In addition, decreased CSF levels of the peptide has been found in Schizophrenia and other neuropsychiatric disorders. 2. In the present work, we have investigated levels of plasmatic somatostatin in a sample of 50 schizophrenic patients compared with a normal control group. 3. Somatostatin was increased in the patient group (p less than 0.01) as a whole but statistical analysis revealed that the increase was associated with the presence of positive symptoms (Factorial Analysis) with a significant correlation, specially with delusion and hallucination scores in the Andreasen rating scales.
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PMID:Plasmatic somatostatin as a marker of positive symptoms of schizophrenia. 134 58

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

Cerebrospinal fluid (CSF) corticotropin releasing hormone (CRH), somatostatin (SRIF), and thyrotropin releasing hormone (TRH) were measured by specific radioimmunoassay methods in 86 patients who met DSM-III-R criteria for schizophrenia or schizophreniform disorder and in 30 neurologic controls. The multivariate CSF peptide concentration was significantly different in patients compared with controls, but none of the individual variable differences reached statistical significance when analyzed separately. There were no significant CSF neuropeptide differences among patients with various schizophrenic subtypes. Neither global severity of illness nor individual symptoms were correlated with CSF neuropeptide concentrations. Although schizophrenic patients showed a pattern of mildly lower SRIF and TRH levels in their CSF, together with a weak tendency for higher CSF CRH values, these peptide changes did not appear to be specifically related to the core features of schizophrenia.
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PMID:CSF corticotropin releasing hormone, somatostatin, and thyrotropin releasing hormone in schizophrenia. 135 93

Cerebrospinal-fluid (CSF) corticotropin-releasing hormone, somatostatin, and thyrotropin-releasing hormone were measured by specific radioimmunoassays in 257 hospitalized psychiatry patients suffering from dementia disorders (n = 85), schizophrenia (n = 104), and mood and anxiety disorders (n = 39). Neurological controls (n = 29) were also investigated. Since there were large overlaps of the peptide levels across the nosological groups we subjected the dataset to a three-dimensional normal mixture distribution analysis. We obtained four biochemically separable clusters. Dementia disorders, but not the others, were heterogeneously distributed in these clusters but after eliminating the effects of age and illness duration this difference disappeared. No single clinical, psychological, or background variable emerged as a prominent correlate of the neuropeptide clusters. It is concluded that although CSF neuropeptide concentrations in psychiatric patient populations appear to be separable into distinct, normally distributed subgroups this distinction does not coincide with present nosological classifications.
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PMID:Cerebrospinal-fluid neuropeptides: a biochemical subgrouping approach. 136 69

1. The tetradecapeptide somatostatin (SS) has a widespread, uneven distribution within several organs including the central nervous system (CNS), with particularly high concentration in the hypothalamus. 2. The SS-related peptides (SS28, SS28(1-12), SS28(15-28)) are originated from the precursor pre-prosomatostatin. 3. SS is suggested to be involved in a large number of CNS functions, locomotion, sedation, excitation, catatonia, body temperature, feeding, nociception, paradoxical sleep, self-stimulation, seizure, learning and memory. 4. SS influences central neurochemical processes. 5. It is possible that SS is related to various neurological and psychiatric illnesses, like Huntington's disease, multiple sclerosis, Parkinson's disease, epilepsy, eating disorders, Alzheimer's disease, schizophrenia and major depressive illness.
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PMID:Preclinical and clinical studies with somatostatin related to the central nervous system. 197 75

Solid-phase IEA was used to measure the level of autoantibodies to somatostatin in the blood serum of 44 schizophrenics and 24 healthy donors. The patients suffering from schizophrenia manifested a higher (p less than 0.01) level of immune responsiveness of the blood serum to somatostatin (0.665 +/- 0.03) as compared to the control group (0.509 +/- 0.05). The main contribution to the differences between the groups as regards the parameter measured is made by patients with malignant (0.810 +/- 0.10) and paranoid (0.773 +/- 0.08) schizophrenia whereas the patients' subgroup with slow-progressive schizophrenia did not differ from normal regarding the level of autoantibodies to somatostatin in the serum (0.504 +/- 0.03). These tentative data agree with a hypothesis of the involvement of autoimmune processes into the development of schizophrenia.
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PMID:[Anti-somatostatin autoantibodies in the blood serum of patients with schizophrenia]. 197 60

Low levels of cerebrospinal fluid (CSF) somatostatin and abnormal response to dexamethasone are two neuroendocrine disturbances reported to appear in depression and other neuropsychiatric disorders. We measured the levels of CSF somatostatin in patients with schizophrenia (n = 44) and depression (n = 19). In view of in vitro and animal evidence of the ability of somatostatin to inhibit stimulated corticotropin secretion, we also administered the dexamethasone suppression test to a subgroup of the patients with schizophrenia (n = 16) and the total depressed group. Lower levels of CSF somatostatin were found in dexamethasone nonsuppressors regardless of diagnosis and were negatively correlated with maximum postdexamethasone cortisol level in the total and depressed patient groups. These data suggest a functional relationship between hypothalamic-pituitary-adrenal axis hyperactivity and reduced CSF somatostatin level.
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PMID:CSF somatostatin and abnormal response to dexamethasone administration in schizophrenic and depressed patients. 286 43

Somatostatin is a tetradecapeptide that is assuming increasing importance as a regulator of central nervous system activity. Originally identified as the hypothalamic growth hormone release-inhibiting factor, somatostatin has subsequently been shown to be extensively and selectively distributed throughout the central nervous system, to alter neuron excitability, to regulate and be regulated by the activity of classical neurotransmitters and neuropeptides, to exert a number of direct behavioral actions, and to display neuropsychiatric disorder-related alterations. In this article, a three-part study of cerebral spinal fluid (CSF) somatostatin in affective illness and schizophrenia is presented. In part 1, significant reductions in CSF somatostatin were observed in 49 bipolar and unipolar depressed patients relative to 47 controls. Values during depression were also significantly lower than those observed in affective disorder during the improved state or in schizophrenia. Diurnal studies involving paired AM and PM lumbar punctures revealed that depressed patients and normal volunteers had similar somatostatin values in the evening, despite having significantly different values in the morning. In part 2, the effects of several psychopharmacological agents on CSF somatostatin were examined, particularly the tricyclic anticonvulsant carbamazepine. A significant reduction of CSF somatostatin during treatment with carbamazepine was observed. The effect of carbamazepine on somatostatin could be related to its anticonvulsant, analgesic, or psychotropic effects. Part 3 deals with somatostatin as a major regulator of hypothalamic-pituitary-adrenal (HPA) axis activity. Somatostatin affects HPA activity by inhibiting, at a number of cellular levels, the stimulated release of adrenocorticotrophic hormone (ACTH) from the pituitary. A significant negative relationship between CSF somatostatin and the postdexamethasone plasma cortisol level in 22 depressed and 16 schizophrenic patients was observed. This relationship between low CSF somatostatin and escape from dexamethasone suppression was observed irrespective of diagnosis (i.e., depression or schizophrenia). Thus, there is indirect supporting evidence for a role for somatostatin dysregulation in the most consistently observed biological abnormality in depression, escape from dexamethasone suppression. Further study of somatostatin in neuropsychiatric disorders, and particularly depressive illness, offers great promise for better understanding their underlying affective, vegetative, cognitive, and physiological dysregulations.
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PMID:Cerebrospinal fluid somatostatin and psychiatric illness. 286 90

Although a biochemical abnormality has been postulated in the etiology of schizophrenia, evidence supporting this hypothesis has been conflicting. Because of the presence of somatostatin-like immunoreactivity (SLI) in limbic system nuclei of the brain, we examined postmortem concentrations of SLI in patients dying with schizophrenia and in normal controls. Concentrations of SLI in Brodmann cortical area 38, hippocampus, caudate, putamen, nucleus accumbens, and both segments of the globus pallidus were not significantly different from controls. In addition, we examined both SLI and neuropeptide-Y-like immunoreactivity (NPYLI) in subnuclei of the amygdala and the substantia innominata. There were no significant alterations in either neuropeptide as compared with controls.
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PMID:Somatostatin and neuropeptide Y are unaltered in the amygdala in schizophrenia. 288 67

The restriction fragment length polymorphisms (RFLPs) associated with neuropeptide Y (NPY) and somatostatin loci were used to assess the possibility of linkage to a locus for affective disorder (AD). When somatostatin haplotypes were assigned to members of 2 AD pedigrees under either rare dominant or recessive transmission, the LOD scores obtained at 0% recombination were inconsistent with linkage. Similar results were obtained with NPY under rare dominant inheritance. Comparison of the frequency of the genotypes deduced from the polymorphic alleles of gastrin-releasing peptide, NPY, somatostatin and substance P in normals vs patients with either AD or schizophrenia suggests the absence of association. The difference in the frequency of the 3.3 kb adenosine deaminase fragment in normals vs bipolar and schizophrenic patients is of borderline significance.
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PMID:Neuropeptide gene polymorphisms in affective disorder and schizophrenia. 289 62


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