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)

Iron status and akathisia were assessed in 105 long-stay in-patients who fulfilled DSM-III-R criteria for schizophrenia, all but three of whom were receiving antipsychotic medication. Chronic akathisia was diagnosed in 23% and pseudoakathisia in 20%. No significant correlation was found between serum iron concentration and the severity of akathisia. There was no significant difference in serum iron concentration between patients with chronic akathisia and those without. However, serum iron and percentage saturation were significantly raised in patients with pseudoakathisia compared with patients with chronic akathisia, and tended to be higher than in patients with akathisia. These findings do not support an association between low serum iron and chronic akathisia.
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PMID:Relationship between iron status and chronic akathisia in an in-patient population with chronic schizophrenia. 136 69

Evidence derived from both pharmacological and postmortem studies suggests that a disturbance of brain iron metabolism is involved in the pathophysiology of schizophrenia; i.e., the distribution of iron parallels that of dopamine, and variations in its brain concentration selectively modulate the binding affinity of the dopaminergic (D2) receptor. In the present study the authors examined the staining intensity of brain iron in postmortem specimens of 9 schizophrenic (SC) patients and 17 age-matched controls. Coronal sections were stained with the Perls's technique, photographed, and then studied using a computerized image analysis system. Optical density measurements were taken from the caudate nucleus, putamen, globus pallidus, and substantia nigra. This study revealed significant differences between groups only for the staining intensity of iron in the caudate nucleus (P less than 0.005). A review of the literature suggests that this finding may be the result of neuroleptic therapy and not a primary pathological feature of schizophrenia.
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PMID:Staining intensity of brain iron in patients with schizophrenia: a postmortem study. 162 59

The role of iron in schizophrenia (SC) has aroused attention because of its modulatory effect on the dopamine receptor and its role as a cofactor for tyrosine hydroxylase. In addition, several postmortem studies suggest that increased mineralization (especially iron) of the basal ganglia is a possible clinicopathological correlate of schizophrenia. In order to quantitate the in vivo mineral content in the basal ganglia of patients with SC, a protocol was developed to analyze CT scans films with a LOATS computer analysis system. A total of 725 consecutive CT scans (275 SC, 450 nonSC) from a psychiatric population were reviewed. Eighteen scans (2.3%) revealed basal ganglia mineralization of which 7 cases carried a diagnosis of SC and 11 had other psychiatric disorders. All subjects had received neuroleptics, and 8 of the 11 patients in the nonschizophrenic group were demented. Both the SC and nonSC patients exhibited a prevalence (2.5%) of basal ganglia mineralization similar to that found in a postmortem series of the general population.
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PMID:No difference in basal ganglia mineralization between schizophrenic and nonschizophrenic patients: a quantitative computerized tomographic study. 201 34

Activity levels of platelet monoamine oxidase (MAO) and plasma amine oxidase (PAO) were determined in eight chronic schizophrenic patients who had been treated with neuroleptic drugs for 3 months. The mean reduction in platelet MAO activity was 18.6%. The extent of decrease was statistically significant. The reduction in enzyme activity was unrelated to serum iron levels. PAO activity was unaltered. The implications for schizophrenia research are discussed.
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PMID:Neuroleptic drug effect on platelet monoamine oxidase and plasma amine oxidase in schizophrenia. 612 54

The total content of zinc in the adult human body averages almost 2 g. This is approximately half the total iron content and 10 to 15 times the total body copper. In the brain, zinc is with iron, the most concentrated metal. The highest levels of zinc are found in the hippocampus in synaptic vesicles, boutons, and mossy fibers. Zinc is also found in large concentrations in the choroid layer of the retina which is an extension of the brain. Zinc plays an important role in axonal and synaptic transmission and is necessary for nucleic acid metabolism and brain tubulin growth and phosphorylation. Lack of zinc has been implicated in impaired DNA, RNA, and protein synthesis during brain development. For these reasons, deficiency of zinc during pregnancy and lactation has been shown to be related to many congenital abnormalities of the nervous system in offspring. Furthermore, in children insufficient levels of zinc have been associated with lowered learning ability, apathy, lethargy, and mental retardation. Hyperactive children may be deficient in zinc and vitamin B-6 and have an excess of lead and copper. Alcoholism, schizophrenia, Wilson's disease, and Pick's disease are brain disorders dynamically related to zinc levels. Zinc has been employed with success to treat Wilson's disease, achrodermatitis enteropathica, and specific types of schizophrenia.
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PMID:Zinc, the brain and behavior. 708 16

The following is a case report of a patient with Sydenham's chorea who later developed schizophrenia. Autopsy examination of this patient revealed mineral deposits in the basal ganglia. The deposition of minerals, especially iron, within subcortical brain structures has been associated with dopaminergic abnormalities, schizophreniform symptoms, and abnormal movement disorders. The psychosis these patients experience is sometimes resistant to treatment with traditional neuroleptics. A CT or MRI scan may prove useful in screening those patients with Sydenham's chorea that develop psychotic symptoms.
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PMID:Sydenham's chorea and schizophrenia: a case report. 754 48

Free radicals are highly reactive chemical species with an unpaired electron, and their formation is catalyzed by transition metals like iron, copper, and manganese. There have been numerous studies linking free radical damage with neuropsychiatric illnesses, including several psychiatric and motor disorders, raising the possibility that antioxidant strategies might serve a neuroprotective role for some conditions. The illnesses studied include tardive dyskinesia, schizophrenia, Parkinson's disease, and Alzheimer's disease. Although oxidative mechanisms may play a role in these conditions, further studies are necessary to define their involvement, and to determine the extent to which antioxidants may partially alleviate or prevent some of these conditions.
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PMID:Free radical involvement in neuropsychiatric illnesses. 767 80

In the last two decades, many biological functions of iron have been identified, in particular its role in many enzymatic processes, its effect on dopamine D2 receptor function, its interaction with other neurotransmitters (gamma-aminobutyric acid, serotonin, opiate-peptides), and its catalytic role in the nonenzymatic mechanisms for oxidation, hydroxylation, and peroxidation reactions. The role of iron in Parkinson's disease, Alzheimer's disease, brain injury due to exogenous causes, neuroleptic-induced movement disorders, schizophrenia, and other neuropsychiatric disorders is currently being explored. This study summarizes current understanding of the anatomy and physiology of brain iron with special reference to these disorders.
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PMID:The neuropsychiatry of brain iron. 809 18

TH is a tetrahydrobiopterin-requiring, iron-containing monooxygenase. It catalyses the conversion of L-tyrosine to L-dopa, which is the first, rate-limiting step in the biosynthesis of catecholamines (dopamine, noradrenaline and adrenaline), the central and sympathetic neurotransmitters and adrenomedullary hormones. The cofactor of TH is tetrahydrobiopterin, which is synthesized from GTP in three steps. The TH gene consists of 14 exons only in humans and 13 exons in animals. Human TH exists in four isoforms (hTH1-4) that are produced by alternative mRNA splicing from a single gene. A single mRNA and protein corresponding to hTH1 exists in non-primates. Monkey TH exists in two isoforms, corresponding to hTH1 and hTH2. TH activity is regulated in the short term by feedback inhibition of catecholamines in competition with tetrahydrobiopterin, and by activation and deactivation due to phosphorylation and dephosphorylation, mainly at Ser-19 and Ser-40 of hTH1. The multiple TH isoforms in humans and monkeys have additional phosphorylation, resulting in more subtle regulation. In long-term regulation under stress conditions, TH protein is induced. CRE and AP1 in the 5' flanking region of the TH gene may be the main functional elements for TH gene expression. TH may be closely related to the pathogenesis of neurological diseases, such as dystonia and Parkinson's disease, psychiatric diseases, such as affective disorders and schizophrenia, as well as cardiovascular diseases. The TH gene may prove useful in gene therapy to compensate for decreased levels of catecholamines in neurological diseases, for example, for supplementation of dopamine in Parkinson's disease.
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PMID:Tyrosine hydroxylase: human isoforms, structure and regulation in physiology and pathology. 882 46

This paper reviews what is currently known about the redox state of the glutamate synapse and its possible role in modulating synaptic plasticity and thus learning and neurocomputation. The hypothesis is presented that the growth or pruning of the synaptic spine is controlled in part by the balance in the synapse between neurodestructive pro-oxidants (e.g., nitric acid radical and hydrogen peroxide) and neuroprotective antioxidants (e.g., ascorbate and carnosine). In addition, there may be a role for catecholamines, in particular dopamine, related to its role in reinforcement signalling. Activation of the dopamine D2 receptor induces the synthesis of an antioxidant enzyme, possibly catalase. Dopamine may also affect the redox balance in the glutamate synapse directly by diffusion from the adjacent dopaminergic bouton-en-passage. Catecholamines are powerful antioxidants, scavengers of free radicals and iron chelators. Catecholamine-iron complexes are potent dismuters of superoxide ions. Additional agents participating in spine pruning may be neurotoxic catecholamine o-quinones present in the brain. This system may be at fault in schizophrenia and Parkinson's disease. Experiments to test the hypothesis are suggested.
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PMID:Redox mechanisms at the glutamate synapse and their significance: a review. 1032 73


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