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)

Birthweight and obstetric complications were registered retrospectively in 24 monozygotic (MZ) twin pairs. Sixteen pairs were discordant and 8 pairs were concordant for DSM-III-R schizophrenia. There was no significant intrapair difference in birthweight between the 2 groups of MZ twins. Prematurity was more often observed in the discordant pairs, but neither differences in prematurity nor differences in obstetric complications between the concordant and discordant twins reached significance. No difference in respect of family history of schizophrenia between the 2 groups of MZ twins was found. In the discordant pairs, no significant difference between the schizophrenic twin and the nonschizophrenic co-twin was observed regarding birth order, birthweight or physical condition at birth.
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PMID:Birthweight and obstetric complications in schizophrenic twins. 154 53

A previous report of cerebral hemiatrophy and schizophrenia added to the list of neurodevelopmental abnormalities associated with schizophrenia. In a new case, the birth history indicated perinatal hemorrhage and prematurity (30-31 weeks of gestation). CT and MR imaging showed reduction in left hemisphere size with ventricular enlargement and mild skull thickening. Loss of periventricular white matter was detected. Changes in skull thickness, size of air cells and volume of the cranial vault may be measurable correlates of putative developmental abnormalities in schizophrenia.
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PMID:Left cerebral hemiatrophy and schizophrenia-like psychosis in an adolescent. 879 14

Psychosis frequently occurs in women of childbearing potential who may have unplanned pregnancies. Understanding the risk of prenatal antipsychotic exposure can be of benefit in selecting therapies. The authors evaluated the in utero and lactation exposure effects of olanzapine, a novel antipsychotic that is used in treating schizophrenia, bipolar disorder, and other conditions and that may have expanded use in the childbearing population. All prospectively and retrospectively ascertained pregnancy reports were collected as a registry in the Lilly Worldwide Pharmacovigilance Safety Database. Outcomes were available from 23 prospectively ascertained olanzapine-exposed pregnancies. Spontaneous abortion occurred in 13%, stillbirth in 5%, major malformation in 0%, and prematurity in 5%, all within the range of normal historic control rates. There were 11 retrospectively ascertained cases of pregnancy. Two retrospectively ascertained cases of lactation exposure did not suggest infant risk. The early experience with olanzapine use in pregnancy and lactation is encouraging in that no obvious added risk to the fetus or infant was observed. Additional cases of pregnancy and lactation exposure need to be evaluated to determine whether these early findings are representative of the risks of olanzapine exposure to the fetus and infant. At this time, olanzapine should only be used during pregnancy and lactation when the potential benefit justifies the potential risk to the fetus or infant.
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PMID:Olanzapine-exposed pregnancies and lactation: early experience. 1091 99

In the general population, low birthweight (LBW) is associated with neurological and psychological problems during childhood and adolescence. LBW may result from premature birth or poor fetal growth, and the independent effects of these two events on childhood development are not fully understood. The rate of low weight births is increased in schizophrenia and is associated with social withdrawal during childhood and an early onset of illness. However, it is unclear whether this LBW reflects poor fetal growth or premature birth, or whether these two risk factors have distinct implications for childhood functioning and age at onset of schizophrenia. Subjects included 270 patients with schizophrenia for whom a detailed history of obstetric events could be obtained. The rate of low weight births was high and was associated with poorer premorbid functioning and an earlier age at illness onset. The rate of both premature births and poor fetal growth was high relative to the normal population. Prematurity, but not poor fetal growth, was associated with premorbid social withdrawal and an early age at illness onset. Poor fetal growth, but not prematurity, was associated with low educational achievement. These results suggest that poor fetal growth and prematurity are associated with distinct patterns of childhood maladjustment in individuals who develop schizophrenia.
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PMID:Low birthweight in schizophrenia: prematurity or poor fetal growth? 1127 35

Mesotelencephalic dopamine (DA) pathways are exquisitely vulnerable to ischemic-anoxic insult. These insults are known to produce long-term derangements in DA signaling and have been hypothesized to contribute, at least in part, to pathologic behaviors such as cerebral palsy, schizophrenia, and attention deficit hyperactivity disorder (ADHD). Whether modest intermittent hypoxia, such as that encountered with repetitive apneas in premature infants, contributes to clinically significant impairments in DA signaling, and how these impairments manifest at a systems level, is unknown. To address these voids there is a need to develop animal models emulating features of a common disorder of prematurity, namely, apnea with hypoxia. Behavioral traits exhibited by such models include disturbed sleep-wake architecture, excessive locomotion, and impaired working memory persisting 1 to 2 months post-insult. Western-blot analysis of expression patterns of proteins involved in DA signaling (e.g., DA and vesicular monoamine transporters, tyrosine hydroxylase, and D1 receptors) are consistent with that which might be expected from hyper- or hypodopaminergic functioning in DA-responsive prefrontal cortex and striatal circuits, respectively. These novel observations suggest that intermittent hypoxia occurring during a period of critical brain development disrupts development of those mesotelencephalic pathways modulating the expression of sleep and wakefulness, locomotion, and executive functioning.
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PMID:Neonatal intermittent hypoxia impairs dopamine signaling and executive functioning. 1252 74

Many pharmacological experiments show that the ionotropic receptor NMDA has both neurotrophic and neuroexcitotoxic effects. The neurotrophic function is manifested in many ways including acceleration of neuronal development, enhancement of neuronal migration, neuroprotection, blockage of apoptosis, prevention of aging and prematurity, as well as effects on synaptic plasticity and synaptogenesis. On the other hand, the neuroexcitotoxic function is manifested in its role in neurological and psychiatric diseases such as epilepsy, Parkinson's disease and schizophrenia. The present study explores the consequences of complete and partial absence of NMDA-NR1 receptors throughout development. Using DiI tracing in vitro, the development of corpus callosum projection neurons in transgenic mice with deletion of the NMDA-NR1 receptor was observed in visual cortex. Compared to littermate controls, the histogenesis and neuronal development of corpus callosum cells of origin was found to be accelerated in NR1-/- mice. That is, the corpus callosum projection neurons in NR1 knockout mice developed earlier and faster than in littermate heterozygous and wild-type mice. However, the corpus callosum projection neurons in NR1 heterozygous mice developed earlier and faster than in littermate wild-type mice. This suggests that NMDA-NR1 receptors are involved in sequencing and/or temporal regulation of neuronal development, and that there is a gene-dose effect. Studies from other laboratories suggest that the observed phenomenon of prematurity or accelerated development is a direct effect of altered expression of genes found in mice with deletion of the NMDA-NR1 receptor.
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PMID:Corpus callosum and visual cortex of mice with deletion of the NMDA-NR1 receptor: I. Accelerated development of callosal projection neurons. 1293 10

Schizophrenia is a multifactorial disease with complex interactions between a genetic liability, possible perinatal complications and exposure to later environmental risk factors in childhood. Maternal influenza infection, wartime-famine-related denutrition and maternal depression or exposure to repeated stress in pregnancy may have a deleterious effect on brain development and neuronal migration. Obstetrical complications which are significantly associated with schizophrenia are bleeding, diabetes, prematurity, fetal growth retardation, Rhesus incompatibility, preeclampsia and congenital malformations. Subjects with onset of schizophrenia before age 22 had more often a history of acute fetal distress (abnormal presentation at birth and complicated cesarean delivery). Obstetrical complications may have a direct negative impact on fetal brain development or may be on the causal pathway between prepartum maternal depression or psychosis, exposure to stress and impaired relation between mother and child consecutive to postnatal depression.
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PMID:[Obstetrical complications and further schizophrenia of the infant: a new medicolegal threat to the obstetrician?]. 1506 96

Human neurodevelopment is the result of genetic and environmental interactions. This paper examines the role of prenatal nutrition relative to psychiatric disorders and explores the relationship among nutrients, mood changes, and mood disorders. Epidemiologic studies have found that adults who were born with a normal, yet low birth weight have an increased susceptibility to diseases such as coronary heart disease, diabetes, and stroke in adulthood. Prenatal caloric malnutrition, low birth weight, and prematurity also increase the risk for neurodevelopmental disorders, schizophrenia, affective disorders, and schizoid and antisocial personality disorders. Placebo-controlled studies in medicated patients suggest that add-on treatment with omega-3 fatty acids, particularly eicosapentaenoic acid, may ameliorate symptoms of major depressive disorder. Additional studies are necessary to confirm any benefits for bipolar disorders.
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PMID:Nutrients, neurodevelopment, and mood. 1553 90

It is suggested that perinatal supplementation of long-chain polyunsaturated fatty acids (LCPUFAs) especially; eicosapentaenoic and docosahexaenoic acids prevent schizophrenia in the adult. I propose that schizophrenia could be a low-grade systemic inflammatory disease with its origins in the perinatal period, probably triggered by maternal infection in a genetically susceptible individual that leads to excess production of pro-inflammatory cytokines both in the mother and the fetus. These cytokines, in turn, induce damage to the fetal neurons leading to the adult onset of schizophrenia. I suggest that maternal infection perse interferes with the metabolism of essential fatty acids (EFAs) resulting in deficiency of LCPUFAs that are known to have neuroprotective action. Alternatively, decreased formation of LCPUFAs as a result of decreased activity of D6 and D5 desaturases (due to prematurity) can result in neuronal damage due to the absence/decrease in the neuroprotective LCPUFAs. This is supported by the observation that LCPUFAs suppress the production of pro-inflammatory cytokines, have anti-inflammatory and neuroprotective actions. Furthermore, LCPUFAs are essential for brain growth and development. If this hypothesis is true, it implies that perinatal supplementation of appropriate amounts of LCPUFAs in the right combination is helpful in the prevention of schizophrenia in adult life.
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PMID:Can perinatal supplementation of long-chain polyunsaturated fatty acids prevents schizophrenia in adult life? 1556 90

Previous investigations of the association of schizophrenia with patterns of pre- and post-natal growth have been based on small numbers of cases or have not taken account of the effects of prematurity on birthweight. We investigated the association of fetal growth with schizophrenia in a large cohort of Swedish males and females. We linked data from the Swedish Medical Birth Register (1973-1980), Inpatient and Discharge Register (1988-2002), Military Service Conscription Register (1990-1997), and the Population and Housing Censuses (1970 and 1990). Altogether 719,476 males and females were followed up from the age of 16 for a mean of 9.9 years. There were 736 incident cases of schizophrenia. Even in models that did not control for gestational age there was little evidence of an association between birthweight and schizophrenia (hazard ratio per kg increase in birthweight: 0.90 (95% CI 0.78 to 1.03); the hazard ratio in babies weighing <2.5 kg compared to 3.5-4.0 kg was 1.29 (95% CI 0.85 to 1.96). There was an inverse association of birth length with schizophrenia across the range of birth lengths. Short babies were at an increased risk (hazard ratio per 10 cm increase in birth length: 0.53, 95% CI 0.31 to 0.89 (fully adjusted model)). All associations were little changed when analyses were restricted to term (>36 week gestation) babies. In males, low body mass index and short height at age 18 were associated with increased risk. There is some evidence that patterns of risk in relation to fetal growth differ depending on post-natal growth patterns: the increased risk associated with low body mass index was restricted to long babies who became light adults. The exposures underlying these associations and the biological mechanisms mediating them require clarification.
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PMID:The association of fetal and childhood growth with risk of schizophrenia. Cohort study of 720,000 Swedish men and women. 1612 3


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