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)

Patients with cerebral atrophy of unknown origin, patients with nuclear forms of schizophrenia or neurosis, and normal subjects were skin-tested with human brain and liver proteins. The frequency of positive delayed skin-sensitivity reactions to brain proteins was significantly higher in the cerebral-atrophy group than in other groups, thus suggesting a correlation between cerebral atrophy and cell-mediated immunity.
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PMID:Cerebral atrophy. An immunological disorder? 6 30

Baseline concentrations of homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA) and MHPG in the cerebrospinal fluid (CSF) were determined in 67 lobotomized and 30 non-lobotomized patients with chronic schizophrenia. In addition, in 69 of these patients the degree of brain atrophy was assessed by a pneumoencephalographic (PEG) technique. There were no significant differences in the concentrations of the monoamine metabolites in the CSF between the two patient groups studied despite the fact that the group of lobotomized schizophrenics had significantly more central and cortical brain atrophy than the group of nonlobotomized schizophrenic patients. The amine metabolite levels were also unrelated to the subtype of schizophrenia, duration of illness, or degree of mental incapacitation.
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PMID:Monoamine metabolite levels in cerebrospinal fluid and brain atrophy in lobotomized schizophrenic patients. 45 76

The authors have observed the evolution of a late catatonic syndrome in a 50 years old woman, without psychological background. They have observed a progressive mental (intellectual) deterioration which have had for a long time a partial and paradoxical aspect, while on the thymic and affective stade an atypical melancolic picture evolved toward a schizophrenic syndrome with catatonic traits which finally came to a stade of marasmus and death after three and a half years of illness. A psychological examination performed at mid course confirmed the mental deterioration without intellectual disorganisation (Wechler) while the Rorschach indicated schizophrenia. The neuro-radiological explorations, repeated several times, have demonstrated the existence of a diffuse cerebral atrophy on the white substance and yet more on the cortex, and it was possible to follow the aggravation of this atrophy. Repeated biological tests were less informative: albumine in the CSF was 0.15 to 0.63 g % and an isolated increase of alpha1-globulines in the CSF was observed at the electrophoresis 4 months before the exitus. Histological examination of cortical biopsies and of the white substance indicates a degenerative encephalopathy with spongiosis and cortical atrophy. Because of the limited value of the histopathological examination, one cannot suggest a systematic interpretation of the catatonic symptoms.
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PMID:[Late catatonic syndrom symptomatic of a degenerative encephalopathy (author's transl)]. 93 Jun 22

Frontal lobe dysfunction is widely suspected to underlie negative symptoms of schizophrenia. This hypothesis is based largely on long-standing observations of the similarities between the effects of frontal lobe lesions and negative symptoms. However, there is little direct evidence specifically for such an association in schizophrenic patients. We measured the relationship between decreased relative prefrontal cortex glucose metabolism (hypofrontality) using positron emission tomography and evaluated the severity of negative symptoms in 20 chronic schizophrenics who underwent scanning while not receiving neuroleptic drugs. We found a close relationship between negative symptoms and prefrontal hypometabolism, particularly in the right dorsolateral convexity. This association was regionally specific. Furthermore, there was no evidence that this relationship was an artifact of age, cerebral atrophy, or severity of positive symptoms.
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PMID:Negative symptoms and hypofrontality in chronic schizophrenia. 136 Feb

Computerized brain imaging techniques have been increasingly used in research into psychiatric disorders. Structural imaging has disclosed subtle brain abnormalities in conditions such as schizophrenia. Functional imaging has shown that metabolic changes in the brain in Alzheimer's disease predate cerebral atrophy and has demonstrated unusual patterns of function in psychotic illnesses.
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PMID:Brain imaging in psychiatry: another look. 154 72

We have previously reported that the activity in platelets of the important antioxidant enzyme glutathione peroxidase (GPx) is inversely correlated with computed tomographic (CT) measures of brain atrophy in a population of patients with chronic schizophrenia, suggesting that low GPx may be a vulnerability factor in those schizophrenic patients with structural brain abnormalities. The significance of this finding has now been explored in a larger clinical population by examining the relation of GPx and CT parameters to psychosocial variables and to the activity of platelet monoamine oxidase (MAO), which has also been reported to be altered in certain schizophrenic populations. In the present study, low platelet GPx and high brain atrophy were found to be associated with DSM-III diagnoses of nonparanoid schizophrenia, a high degree of chronicity, and a predominance of negative symptoms. Contrary to some literature reports, atrophy also correlated with age and length of illness among the schizophrenic patients, although the contribution of these factors was less than that of low GPx, which was itself not age dependent. The ventricle-brain ratio (VBR) and atrophy were highly correlated in a control group of affective disorder patients, but not in the schizophrenic group, where large VBRs were found predominantly in the DSM-III undifferentiated subgroup. The low-GPx/high-atrophy schizophrenic patients had normal platelet MAO levels, and MAO was significantly lower only in the paranoid subgroup, consistent with reported observations. There was no evidence for a neuroleptic-induced effect on either enzyme.
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PMID:Platelet glutathione peroxidase and monoamine oxidase activity in schizophrenics with CT scan abnormalities: relation to psychosocial variables. 196 70

Thirty-one patients with schizophrenia and 33 normal control subjects underwent MRI. The BPRS was used to rate clinical symptoms and the NART to estimate pre-morbid IQ. All were right handed. The temporal lobe was significantly smaller on the left than the right in both the control and schizophrenic groups. The amygdala was smaller on the left than the right in controls but not in schizophrenics. The parahippocampal gyrus was smaller on the left side in the schizophrenic group but not in controls. In the schizophrenic group, ventricular enlargement and cerebral atrophy were significantly related to severity of symptoms. Patients with marked negative symptoms had a bilateral reduction in the size of the head of caudate and the two measures were significantly correlated. Patients with marked positive symptoms had larger VBRs and again the clinical and morphometric changes were significantly correlated. There were no morphometric differences between patients with short duration (two years or less) and chronic symptoms.
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PMID:A magnetic resonance imaging study of schizophrenia: brain structure and clinical symptoms. 201 5

It has long been suggested that abnormal functions of the pineal gland may be implicated in the pathophysiology of schizophrenia. We present evidence proposing that diminished melatonin secretion may be associated with the pathophysiology of a subgroup of schizophrenic patients characterized by cerebral atrophy and ventricular enlargement, negative symptoms, impaired cognitive and psychosexual development, onset at pubescence, poor response to neuroleptic medication, and possible increased risk of extrapyramidal symptoms. This view holds that a subnormal plasma melatonin level may be a marker of a subgroup of schizophrenia and may also denote a specific genetic susceptibility.
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PMID:Pineal melatonin in schizophrenia: a review and hypothesis. 207 42

Tc-99m hexamethylpropylene amineoxime (HMPAO) was used to image cerebral perfusion changes in 20 patients with chronic schizophrenia (19 male and 1 female, aged 22-48, at an average age of 29.0). All were being given neuroleptic drugs. Twelve had electroconvulsive therapy. In addition, all had abnormal studies except one, who was normal and had a poor response to treatment. Ventricular dilatation and cerebral atrophy was seen in eleven patients, and 77 focal lesions were detected. Forty-two lesions demonstrated increased HMPAO retention, which was distributed as follows: 26 in the basal ganglia in 14 patients (12 bilateral, 2 unilateral); 10 along the sylvian fissure in the parietotemporal region; and 3 in the frontal and 1 in each of the temporal, parietal, and occipital regions. Thirty-five focal lesions exhibited decreased perfusion: ten parietal, eight frontal, seven temporal, six cerebellar, and four occipital lobes. This study demonstrates the potential value of Tc-99m HMPAO in schizophrenia and other psychiatric disorders.
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PMID:Cerebral perfusion changes in schizophrenic patients using Tc-99m hexamethylpropylene amineoxime (HMPAO). 238 38

The binding of [3H]nipecotic acid, a ligand for labelling GABA uptake sites in brain, was measured in left and right frontal cortex, polar temporal cortex, hippocampus and amygdala from control and schizophrenic postmortem brains. In schizophrenic brains, single concentration [3H]nipecotic acid binding was reduced bilaterally in amygdala and hippocampus and on the left side only in polar temporal cortex. These data suggest that GABA neurones are involved in the cerebral atrophy of schizophrenia and, in agreement with other studies, that this process is most pronounced in left temporal cortex.
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PMID:Reduced GABA uptake sites in the temporal lobe in schizophrenia. 261 32


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