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)

The effect of zinc nutriture and metabolism on brain function has been reviewed. Zinc nutriture and its effect on the concentration and metabolism of essential elements (e.g. zinc, copper, manganese, magnesium, sodium, potassium and calcium) and on the concentration and metabolism of toxic elements (e.g. aluminum and lead) are discussed in relationship to brain function. In addition, possible interrelationships between zinc nutriture and metabolism and its effect on a number of diseases including acrodermatitis enteropathica, Pick's disease, Alzheimer's disease, schizophrenia, fifth day fits, and epilepsy are discussed. Descriptions and comparisons of methods to measure brain zinc are presented. Behavioral changes and the altered brain morphology which have been associated with zinc deficiency are reviewed. Some possible mechanisms for the association of anorexia with zinc deficiency are outlined. Perinatal brain damage produced by early zinc deficiency followed by rehabilitation with adequate zinc appears to be long term, maybe permanent. Interrelationships between zinc nutriture and aspects of neurochemistry are outlined. Some of the neurochemistries discussed include nucleic acid and protein synthesis, cytoskeletal proteins, neurotransmitters (e.g. catecholamines, indoleamines, glutamate, gamma-aminobutyric acid, and neuropeptides), neurotransmitter receptors, 7S nerve growth factor and zinc-binding proteins. Recent evidence linking zinc and neurotransmission is discussed.
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PMID:Zinc and the central nervous system. 330 3

Methods for localizing functional polymorphisms in candidate genes are important for the elucidation of pathogenesis in complex diseases such as schizophrenia and manic depression. Temperature gradient gel electrophoresis (TGGE), a variant of denaturing gradient gel electrophoresis (DGGE), can detect single-base mutations in a specified region of double-stranded DNA. This technique has been evaluated for use with polymerase chain reaction (PCR)-generated DNA fragments containing either transitional (A to G) or transversional (T to A) mutations. Single-base mutations of both types are detectable in PCR fragments up to 500 bp long. This method was then used to examine the coding region of the beta-nerve growth factor (NGF) gene for polymorphisms in PCR-generated DNA fragments derived from lymphocyte DNA of subjects with schizophrenia and normal subjects. No single-base mutations in sequence coding for the mature beta-NGF peptide were found in any of the subjects who were examined. If DNA sequence information is available for PCR primer design, TGGE detection of DNA polymorphisms can be used to rapidly determine whether or not a defect in a gene of interest contributes to the pathophysiology of the illness.
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PMID:Temperature gradient gel electrophoresis analysis of the beta-NGF gene in schizophrenia. 778 81

The level of autoantibodies (AAB) to nerve growth factor (NGF) was examined in blood of mentally healthy children, children with early children schizophrenia as well as with Kanner's and Asperger's syndromes too. The elevated titer of AAB to NGF was determined in blood of children with acute, active state of disease; meanwhile the same titer wasn't changed in the state of stable remission or steady defective state as compared with control group. The correlation was found between the level of AAB to NGF and the degree of disease progression. The correlations which were revealed between AAB to NGF level and peculiarities of the clinical state of patients permitted to use this index as the objective marker of both the acuteness and the severity of the patient's state.
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PMID:[An elevation in the level of autoantibodies to nerve-growth factor in the blood serum of schizophrenic children]. 916 49

A study was made of 54 patients with different forms of schizophrenia: paranoid (8), shift-like (30), slow-progredient (16). According to ICD-10 the rubrics were: F20.00 and F20.01; F20.22 and F20.02; F21 respectively. Elevation of the level of autoantibodies (aAB) to nerve growth factor (NGF) 1,5-fold was registered in blood serum of schizophrenic patients by means of enzyme immunoassay as compared with 70 healthy controls. The dependence of aAB level upon the stage of the disease development was found: in the active phase there was a significant increase of aAB level as compared with the patients in remission (1.38 +/- 0.26 and 0.92 +/- 0.25 units of optical density, respectively). There were no differences in respect of different forms of disease. The authors suggest to use aAB level as the index of the disease activity.
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PMID:[Changes in the level of autoantibodies to the nerve growth factor in the blood serum of schizophrenia patients]. 957 28

There is increasing evidence that a neurodevelopmental process is accountable for at least a proportion of schizophrenic cases. Brain-derived neurotrophic factor (BDNF), a member of a group of proteins that includes neurotrophin-3/4/5 and nerve growth factor (NGF), is an attractive candidate gene. We have performed a case control association study using the BDNF dinucleotide repeat polymorphism in a sample of familial schizophrenic individuals and in healthy, ethnically matched control subjects. We also performed a linkage analysis on 265 multiplex families using the same marker. We found no differences in allele frequencies between the patient and control groups nor any evidence for transmission disequilibrium or linkage with the multiply affected families. We conclude that DNA variation at or near the BDNF gene is unlikely to contribute to the genetic predisposition to schizophrenia.
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PMID:No linkage or linkage disequilibrium between brain-derived neurotrophic factor (BDNF) dinucleotide repeat polymorphism and schizophrenia in Irish families. 985 28

A level of autoantibodies (aAB) to nerve growth factor (NGF) was measured in blood serum of children from 4 groups: 1) schizophrenic patients; 2) children from the families, in which one of the parents suffered with schizophrenia (high risk groups of schizophrenia); 3) children with residual-organic damages of CNS; 4) control group. This index was also determined in their mothers. Significant elevation of a titer of aAB to NGF was observed in blood of children from groups 1 and 2 as well as in their mothers, as compared with 3 and 4 groups. Among the mothers of the children from 1 and 2 groups there were met women with different endogenous mental disorders, with the disorders of personality as well as mentally healthy women. An increase of a level of aAB to NGF was found in all the women from groups 1 and 2, independently of their mental status including mentally healthy women. Such results allow to consider elevated level of aAB to NGF as a risk factor of mental pathology.
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PMID:[Nerve growth factor auto-antibodies in the sera of mothers of schizophrenic children and children from high risk group]. 1020 43

It has been hypothesized that a deleterious key contribution to schizophrenia (SZ) development is a failure of migration and setting of young neurons into their appropriate cortical target sites, particularly in the entorhinal cortex (EC). To test this hypothesis in an animal model, we injected, in pregnant rats, on gestational day (GD) 9, or 10, or 11, or 12, the antimitotic compound methylazoxymethanolacetate (MAM) known to cause EC neuronal loss. We investigated whether or not EC disruption during prenatal development is able to affect behavior, including memory and learning, and brain nerve growth factor (NGF). Prenatally MAM treated young rats didn't display gross behavioral changes in social interaction, open-field and novel object investigation tests. By contrast, GD11 and GD12 MAM treated rats had a retardation in passive avoidance acquisition, while, in GD12 animals, pain sensitivity was reduced. GD12 animals also showed increased NGF in the EC and remaining cortex. MAM treated animals showed no changes in paw NGF or substance P levels suggesting that the altered nociceptive response is not related to local downregulation of these two molecules. The possibility that these behavioral and biochemical alterations might be associated with the onset of SZ is discussed.
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PMID:Prenatal methylazoxymethanol acetate alters behavior and brain NGF levels in young rats: a possible correlation with the development of schizophrenia-like deficits. 1046 89

Studies were performed on 54 patients with different types of schizophrenia-paranoid (8), recurrent-progressive (30), and slowly progressive (16), with ICD-10 rubrics F20.00 and F20.01, F20.22 and F20.02, and F21 respectively. An immunoenzyme method was used to demonstrate that schizophrenia patients had elevated levels of autoantibody to nerve growth factor, by a factor of 1.5 compared with a group of 70 healthy subjects. The autoantibody level was related to the stage of disease: during the active phase, there was a significant increase compared with patients in remission (1.38 +/- 0.26 and 0.92 +/- 0.25 U respectively). There were no differences between variants with different disease courses. The authors suggest that the data obtained here indicate that the autoantibody level can be used as a measure of the activity of the disease process.
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PMID:Changes in the serum levels of autoantibody to nerve growth factor in patients with schizophrenia. 1049 50

It is well known that the nucleoside adenosine exerts a modulatory influence in the central nervous system by activating G protein coupled receptors. Adenosine A2A receptors, the subject of the present review, are predominantly expressed in striatum, the major area of the basal ganglia. Activation of A2A receptors interferes with effects mediated by most of the principal neurotransmitters in striatum. In particular, the inhibitory interactions between adenosine acting on A2A receptors and dopamine acting on D2 receptors have been well examined and there is much evidence that A2A receptors may be a possible target for future development of drugs for treatment of Parkinson's disease, schizophrenia and affective disorders. Our understanding of the role of striatal A2A receptors has increased dramatically over the last few years. New selective antibodies, antagonist radioligands and optimized in situ hybridization protocols have provided detailed information on the distribution of A2A receptors in rodent as well as primate striatum. Studies on the involvement of A2A receptors in the regulation of DARPP-32 and the expression of immediate early genes, such as nerve growth factor-induced clone A and c-fos, have pointed out an important role for these receptors in regulating striatopallidal neurotransmission. Moreover, by using novel selective antagonists for A2A receptors and transgenic mice lacking functional A2A receptors, crucial information on the behavioral role of striatal A2A receptors has been provided, especially concerning their involvement in the stimulatory action of caffeine and the anti-Parkinsonian properties of A2A receptor antagonists. In the present review, current knowledge on the distribution, biochemistry and function of striatal A2A receptors is summarized.
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PMID:Distribution, biochemistry and function of striatal adenosine A2A receptors. 1050 34

The central nervous system is increasingly being recognised as a target organ for vitamin D via its wide-ranging steroid hormonal effects and via the induction of various proteins such as nerve growth factor. This paper proposes that low maternal vitamin D may impact adversely on the developing foetal brain, leaving the affected offspring at increased risk of adult-onset schizophrenia. The hypothesis can parsimoniously explain diverse epidemiological features of schizophrenia, such as the excess of winter births, increased rates of schizophrenia in dark-skinned migrants to cold climates, the increased rate of schizophrenia births in urban versus rural setting, and the association between prenatal famine and schizophrenia. Studies that will allow rejection of the hypothesis are proposed.
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PMID:Hypothesis: is low prenatal vitamin D a risk-modifying factor for schizophrenia? 1063 55


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