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)

Changes in brain structure have been demonstrated in elderly patients suffering affective disorder. Enlarged ventricles are associated with cognitive impairment and higher mortality. Depressed subjects also may show a greater degree of cortical atrophy and subcortical white matter, and basal ganglia lesions seem to be commoner than in age-matched controls. The abnormalities demonstrated are not as severe as those found in degenerative dementias such as Alzheimer's disease, and at present there is no evidence to suggest they are progressive. There is a convincing association with vascular disease, although further neuropathologic correlates are needed. Functional imaging methods are just beginning to be applied to elderly populations and, in affective disorder, findings are similar to those in younger patient groups. The results from different groups vary due to technologic differences and the clinical heterogeneity of the patients studied. Depression, however, may be accompanied by decreased and mania by increased cerebral blood flow or metabolism. Evidence also appears to be mounting of a state-dependent frontostriatal dysfunction in depression. Challenges for the future include replicating such results using larger diagnostically homogeneous patient groups and differentiating the findings from those in other disorders such as schizophrenia and basal ganglia disorders.
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PMID:Imaging and affective disorder in the elderly. 160 Apr 77

The neuropathological results from a prospective, systematically assessed, series of 56 schizophrenic patients and 56 age- and sex-matched normal controls have been presented. When compared with the normal controls, the brains of the schizophrenic subjects showed a significant reduction in brain weight and brain length with a concomitant increase in ventricular size. (All findings relate to measurements made after formalin fixation). In addition, the brains of the schizophrenic patients contained significantly more non-specific focal pathology and fibrillary gliosis than the controls. After exclusion of cases with moderate and severe Alzheimer-type change, cerebro-vascular disease and all forms of focal pathology, the structural brain changes (i.e. decrease in brain weight and brain length) continued to distinguish the schizophrenia group from the controls. Furthermore, an analysis of the clinical data showed that the structural brain changes were correlated in the schizophrenic patients with a measurement of pre-morbid function. The findings and their possible aetiological implications have been discussed.
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PMID:Schizophrenia and the brain: a prospective clinico-neuropathological study. 235 55

The author studies 109 patients with schizophrenia combined with cerebrovascular pathology (vegetovascular crises, essential hypertension, cerebral atherosclerosis). The effect of vascular disorders on the clinical picture and course of different forms of schizophrenia was found to be heterogeneous, being dependent on the severity of vascular disease, as well as the type of the course and progression of the schizophrenic process. Changes in the psychopathological structure of schizophrenic manifestations were the greatest in patients with periodic, shift-like, and slowly progressive schizophrenia.
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PMID:[Effect of vascular pathology on the clinical picture of schizophrenia]. 382 75

1. A sample of 165 schizophrenic subjects was compared to a normal control group in order to evaluate associations between white matter hyperintensity signals and vascular risk factors. 2. A comprehensive medical chart review was completed on all subjects evaluating potential vascular risk factors. Brain MRI acquisition was performed with 0.5 and 1.5 Telsa Philips scanners. 3. Prevalence rates of WMH signals in schizophrenic subjects and normal controls were 4.8% and 4.9%, respectively. 4. A significant association was found for schizophrenics with WHM signals to schizophrenics without signals for hypertension and history of CVA's. 5. This finding is consistent with an etiology of WMH signals in schizophrenia being related to vascular disease.
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PMID:White matter hyperintensity signals associated with vascular risk factors in schizophrenia. 770 30

We had already made a report on outcome of schizophrenia (1986). The patients, 129 typical schizophrenia, were continuously observed over 30 years in the Kawagoe Dojinkai Hospital. Recently, we again evaluated their prognoses according to the same criteria as adopted in the first report, and divided them into the following five groups. [symbol: see text]: completely remitted group (21 persons, 16.3%), [symbol: see text]: almost remitted cases now holding jobs (23 persons, 17.8%), [symbol: see text]: Slightly remitted group showing good adjustment at home or hospital (41 persons, 31.8%), [symbol: see text]: maladjusted cases always showing an unfavorable condition (25 persons, 19.4%), x : incurable cases (19 persons, 14.7%). 1) In the last 8 years, there were 30 persons (23.3% of the whole patients) who showed prognostic changes (10 persons improved, 20 persons worsen). While the second group ([symbol: see text]) has seen fewer persons (12 persons down) than previous study, the third group ([symbol: see text]) has seen more persons (9 persons up). Each three groups, that is, the first two groups ([symbol: see text] + [symbol: see text], 44 persons, 34.1%), the third group ([symbol: see text], 41 persons, 31.8%), and the forth and fifth groups ([symbol: see text] + x, 44 persons, 34.1%) accounted for a third of the whole patients. It is after 32 years on the average (extending from 21 to 50 years) from the onset of illness that they showed prognostic changes. 2) Generally speaking, catatonic patients had favorable prognoses, hebephrenic patients unfavorable ones, and paranoid patients medium ones. But 4 improved persons in the forth and fifth groups were all hebephrenic type. 3) 17 among the 30 persons who showed prognostic changes were unstable type. They took a wave-like course. 4) 27 of all the 129 patients were dead. 25 were dead from disease mentioned below. Malignancy (8 persons), Cerebral vascular disease, Pneumonia and Diabetes (3 persons), Heart-failure (2 persons), Ileus, Myocardial infarction, Hepato-cirrhosis, Gastric ulcer, Tuberculosis and Natural death (1 person). 2 persons committed suicide. 5) Outcome of 45 patients who discontinued our medical therapy became clear as follows. [symbol: see text] + [symbol: see text]: 18 persons (40.0%), [symbol: see text]: 9 persons (20.0%), [symbol: see text] + x : 18 persons (40.0%). A smaller percentage of the patients belongs to the third group ([symbol: see text]) than that of our patients who were continuously followed by us.
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PMID:[Outcome of schizophrenia--extended observation (more than 30 years) of 129 typical schizophrenic cases [III]]. 773 53

Psychosomatic theories suggest that psychiatric pathology modulates mortality rates; some diagnoses could be considered as risk factors and others as protective factors regarding the different causes of death. The results obtained so far are controversial. The present study aimed at determining the associations between psychiatric diagnosis and cause of death on the basis of 1698 deaths which occurred in a regional Swiss psychiatric hospital during the 1945-1989 period. The diagnoses were divided into four groups (psycho-organic syndromes/dysthymia/schizophrenia/others) and the causes of death into five groups (cardiovascular/lung diseases/cancer/suicide/others). As data were lacking for the entire group of hospitalized patients, associations were analyzed by way of a proportional approach (PMR). The proportional variation factors attributed to a given cause were studied by logistic regression (case-control design). The results mainly reveal the specificity of dysthymic patients which were characterized by a decreasing proportion of deaths due to pulmonary diseases and an increasing proportion of deaths due to cardio-vascular disease. Suicide was proportionally more frequent in both dysthymic and schizophrenic patients. The classic hypothesis that schizophrenics are protected against cancer was not confirmed. The limits of the proportional approach (PMR) are discussed.
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PMID:[Psychiatric diagnosis and cause of death in a hospitalized population]. 820 79

Homozygous mutation of the thermolabile variant of methylene tetrahydrofolate reductase (MTHFR) may result in hyperhomocystinemia, leading to an increased risk for early cardiovascular disease, neural tube defects, and possibly major depression, schizophrenia. According to recent studies heterozygosity for the thermolabile variant of the MTHFR gene mutation is also more frequent in patients with thrombotic disease compared to that in the average population. We report on a family with different types of early vascular disease. In four consecutive generations MTHFR heterozygosity was detected: in the proband and in her mother, grandfather and daughter. Further conditions of the family members, possibly due to carrying the mutation, came to light by the pedigree analysis and examinations. The patient had pulmonary emboli at young age, her aunt died of spina bifida shortly after birth. The patient's mother suffers from schizophrenia and depression. The grandfather had pulmonary emboli, her sister with spina bifida occulta also carries the same mutation, as does her daughter who is sofar asymptomatic. In other asymptomatic members of the family no mutations were found. Unexpectedly, hyperhomocystinemia was detected in all heterozygote individuals. Our study demonstrates the necessity for folic acid therapy in mutation carriers to prevent early vascular events, depression and schizophrenia, and also to reduce the risk for neural tube defects in a preconception setting.
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PMID:[Vascular diseases, spina bifida and schizophrenia in a single family associated with the heterozygote mutation of the heat-sensitive variant of methylenetetrahydrofolate reductase]. 1148 7

Homocysteine is a neurotoxic amino acid originally found to be an independent risk factor for cardiovascular and cerebral vascular disease and more recently suggested to be a risk factor for Alzheimer's disease. Several authors have observed high plasma homocysteine levels among schizophrenia patients. We reported that such high levels characterize young male schizophrenia patients. We now studied two groups of schizophrenia patients (N=41) and controls (N=29) for CSF homocysteine levels. No difference was found for CSF homocysteine levels between schizophrenia patients and controls (p=.041 for Study A and p=.52 for Study B).
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PMID:CSF homocysteine is not elevated in schizophrenia. 1565 44

Elevated plasma homocysteine has been found to be a risk factor for Alzheimer's disease as well as cerebral vascular disease, suggesting that some risk factors can accelerate or increase the severity of several CNS disease processes. We screened plasma total homocysteine levels of 193 schizophrenic patients vs. 762 controls for plasma homocysteine levels. The effect of schizophrenia was marked (p<0.0001) and mean homocysteine level was 16.3+/-12 (S.D.) microM in schizophrenic patients vs. 10.6+/-3.6 (S.D.) microM in healthy controls. The increase was almost entirely in young male schizophrenic patients. It seemed important to determine if this finding is already present in newly admitted schizophrenic patients. Serum homocysteine levels were studied in 184 consecutively admitted schizophrenic patients and 305 control subjects. Homocysteine levels were markedly increased in this population of newly admitted schizophrenic patients, especially in young males. However, no difference was found for CSF homocysteine levels between schizophrenia patients and controls. We also examined homocysteine levels in 41 euthymic outpatients with bipolar disorder. Functional deterioration in patients was rated as 'present' or 'absent' by consensus of two treating clinicians. Young male bipolar patients were found to have higher homocysteine levels than controls. Among the male subjects, bipolar patients showing deterioration had homocysteine levels which were significantly higher than other patients. We attempted to develop a model of homocysteine neurotoxicity in mice. Mice were fed homocysteine in water at a dose of 200 mg/kg per mouse per day. Independent samples of animals were studied at 2 to 6 months with behavioral tests including apomorphine-induced stereotypy and spatial learning and memory in the Morris Water Maze. Homocysteine levels were elevated up to 800% at months 5 and 6 by this procedure. No homocysteine-induced defects were found in any behavioral test until month 5 when mild but statistically significant abnormalities in the Morris Water Maze were detected.
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PMID:High homocysteine serum levels in young male schizophrenia and bipolar patients and in an animal model. 1611 16

A disturbed methylation has been proposed as a mechanism via which homocysteine is associated with diseases like vascular disease, neural tube defects and mental disorders. Catechol-O-methyltransferase (COMT) is involved in the S-adenosylmethionine-dependent methylation of catecholamines and catecholestrogens and in this way contributes to homocysteine synthesis. COMT dysfunction has been related to schizophrenia and breast cancer. We hypothesized that COMT dysfunction by virtue of functional genetic polymorphisms may affect plasma total homocysteine (tHcy). Our primary objective was to study the association between common COMT polymorphisms and tHcy. Secondly, we evaluated these polymorphisms as a risk factor for recurrent venous thrombosis. We obtained genotype data from four polymorphisms in the COMT gene (rs2097603, rs4633, rs4680 [324G>A] and rs174699) from 401 population-based controls. We performed haplotype analysis to investigate the association between common haplotypes and tHcy. In addition, we assessed the rs4680 variant as a genetic risk factor in a case-control study on recurrent venous thrombosis (n = 169). We identified a common haplotype that was significantly associated with tHcy levels. This effect was largely explained by the rs4680 variant, resulting in an increase in tHcy of 10.4% (95% CI 0.01 to 0.21, p = 0.03) for 324AA compared with 324GG subjects. Interestingly, we found that the 324AA genotype was more common in venous thrombosis patients (OR 1.61 [95% CI 0.97 to 2.65], p = 0.06) compared to control subjects. We show that the COMT rs4680 variant modulates tHcy, and might be associated with venous thrombosis risk as well.
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PMID:Catechol-O-methyltransferase genotype is associated with plasma total homocysteine levels and may increase venous thrombosis risk. 1806 18


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