SEARCH · PubMed Health

Results for “Neurodevelopment”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 559 records · Page 31Linked to original sources

PubMedDate not supplied

Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children.

Because of the growing concern that exposures to airborne pollutants have adverse effects on fetal growth and early childhood neurodevelopment, and the knowledge that such exposures are more prevalent in disadvantaged populations, we assessed the joint impact of prenatal exposure to environmental tobacco smoke (ETS) and material hardship on the 2-year cognitive development of inner-city children, adjusted for other sociodemographic risks and chemical exposures. The purpose was to evaluate the neurotoxicant effects of ETS among children experiencing different degrees of socioeconomic disadvantage, within a minority population. The sample did not include children exposed to active maternal smoking in the prenatal period. Results showed significant adverse effects of prenatal residential ETS exposure and the level of material hardship on 2-year cognitive development, as well as a significant interaction between material hardship and ETS, such that children with both ETS exposure and material hardship exhibited the greatest cognitive deficit. In addition, children with prenatal ETS exposure were twice as likely to be classified as significantly delayed, as compared with nonexposed children. Postnatal ETS exposure in the first 2 years of life did not contribute independently to the risk of developmental delay, over and above the risk posed by prenatal ETS exposure. The study concluded that prenatal exposure to ETS in the home has a negative impact on 2-year cognitive development, and this effect is exacerbated under conditions of material hardship in this urban minority sample.

Child↗

PubMedDate not supplied

Developmental chlorpyrifos effects on hatchling zebrafish swimming behavior.

Chlorpyrifos (CPF), a widely used organophosphate insecticide and potent acetylcholinesterase inhibitor, interferes with neurobehavioral development. Rat models have been key in demonstrating that developmental CPF exposure causes learning deficits and locomotor activity alterations, which persist into adulthood. Complementary nonmammalian models can be useful in determining the neurodevelopmental mechanisms underlying these persisting behavioral effects. Zebrafish (Danio rerio) with their clear chorion and extensive developmental information base provide an excellent model for assessment of molecular processes of toxicant-impacted neurodevelopment. We have developed methods for assessing spatial discrimination learning in adult zebrafish and have documented persisting effects of developmental CPF exposure on swimming activity and learning after low and high doses of CPF (10 and 100 ng/ml) administered to zebrafish embryos on Days 1-5 postfertilization (pf). In the current study, we developed methods for behavioral assessment of CPF exposure on swimming activity in newly hatched zebrafish. An equal area segmented annular grid (concentric circles divided into quadrants through the diameter) was made in a 16-mm diameter cylinder. The test area was placed on a heating device secured to an Olympus SZH10 dissecting scope stage. Zebrafish embryos were exposed to 10 ng/ml CPF, 100 ng/ml CPF, or vehicle control (25 microl/ml DMSO) (n=8-10/treatment group). Each treatment group was kept in a total volume of 25 ml of egg water (60 mg/ml Instant Ocean) including DMSO with or without CPF mixed to above dilutions in an incubator set at 28.5 degrees C. CPF dilutions or vehicle were changed daily with exposure ending on Day 5 pf. Testing of larval zebrafish was performed on Days 6 and 9 pf. The fish were placed in the test cylinder with 1.5 ml of egg H(2)O (28.5 degrees C). After a 2-min acclimation period, the swimming activity of the fish was measured for a 3-min testing session. The 100 ng/ml CPF dose caused significant slowing of swimming activity on Days 6 and 9 pf and had persisting effects of impairing spatial discrimination and decreasing response latency in adulthood. Developmental exposure to 10 ng/ml of CPF did not cause a significant change in locomotor activity during the period soon after hatching. CPF exposure during early development caused clear behavioral impairments detectable during the posthatching period. In a previous study, we found that early developmental CPF exposure caused behavioral alterations in zebrafish, which lasted throughout adulthood. The molecular mechanisms by which early developmental CPF exposure produces these behavioral impairments expressed in adulthood can now be studied in the zebrafish model.

Animals↗

PubMed2003

Bilirubin toxicity in the developing nervous system.

Bilirubin toxicity remains a significant problem despite recent advances in the care of jaundiced (hyperbilirubinemic) neonates. A recent surge in reported cases of classical kernicterus, due in part to earlier hospital discharge and relaxation of treatment criteria for hyperbilirubinemia, and new reports of hyperbilirubinemia-induced auditory dysfunction using evoked potential based infant testing and hearing screening, underscore the need to better understand how hyperbilirubinemia causes brain damage in some infants, especially because the damage is preventable. Recent progress in understanding bilirubin binding and neurotoxicity resulting from unbound or "free" unconjugated bilirubin, how bilirubin affects the central nervous system in vivo and in vitro, and the use of new clinical tools in neonates, for example magnetic resonance imaging revealing bilateral lesions in globus pallidus and subthalamus, and abnormal brainstem auditory evoked potentials with normal inner ear function, may lead to improved detection and prevention of neurologic dysfunction and damage from bilirubin. Finally, the concern is raised that partial or isolated neurologic sequelae, for example auditory neuropathy and other central auditory processing disorders, may result from excessive amount and duration of exposure to free, unconjugated bilirubin at different stages of neurodevelopment.

Animals↗

PubMed2003

Glutamatergic neurotransmission modulation and the mechanisms of antipsychotic atypicality.

The neurotransmission mediated by the excitatory amino acids (EAA) glutamate (GLU) and aspartate is of interest to the pharmacotherapy of psychosis due to its role in neurodevelopment and neurotoxicity, its complex interactions with dopaminergic and other neurotransmitter systems and its pivotal importance in recent models of schizophrenia. Accumulating evidence indicates that modulation of glutamatergic neurotransmission may play an important role in the mechanisms of action of atypical antipsychotic drugs. The principles of the phencyclidine (PCP) model of schizophrenia suggest that conventional neuroleptics cannot counteract all aspects of schizophrenia symptomatology, while a more favorable outcome, including anti-negative and cognitive symptoms effects, would be expected with the use of treatment modalities targeting glutamatergic neurotransmission. Clozapine and other presently used atypical antipsychotics differ from conventional neuroleptics in the way they affect various aspects of glutamatergic receptors function. In this context, a specific hypothesis suggesting an agonistic role of clozapine at the N-methyl-D-aspartate (NMDA) subtype of GLU receptors has been postulated. Furthermore, the results of the first generation of clinical trials with glycine (GLY) site agonists of the NMDA receptor in schizophrenia suggest that this type of compounds (1) have efficacy and side effects profiles different than those of conventional neuroleptics and (2) differ in their synergic effects when used in addition to conventional neuroleptics versus clozapine and possibly additional atypical antipsychotics. These findings (1) bring further support to the hypothesis that glutamatergic effects may play an important role in the mechanism of action of atypical antipsychotics, (2) help explain the unique clinical profile of clozapine, and (3) suggest that GLY site agonists of the NMDA receptor may represent a new class of atypical antipsychotic medication. Future research in this area is bound to bring about a better understanding of the role of glutamatergic neurotransmission manipulation in the pharmacotherapy of psychosis and the development of novel pharmacological strategies targeting GLU brain systems.

Animals↗

PubMed2005

Apoptotic mechanisms in the pathophysiology of schizophrenia.

While schizophrenia is generally considered a neurodevelopmental disorder, evidence for progressive clinical deterioration and subtle neurostructural changes following the onset of psychosis has led to the hypothesis that apoptosis may contribute to the pathophysiology of schizophrenia. Apoptosis (a.k.a. programmed cell death) is a mechanism of cell death that operates in normal neurodevelopment and is increasingly recognized for its role in diverse neuropathological conditions. Activation of apoptosis can lead to rapid and complete elimination of neurons and glia in the central nervous system. Studies also show that in certain settings, pro-apoptotic triggers can lead to non-lethal and localized apoptotic activity that produces neuritic and synaptic loss without causing cell death. Given that the neuropathology of schizophrenia is subtle and includes reduced neuropil (especially synaptic elements), limited and often layer-specific reductions of neurons, as well as neuroimaging data suggesting progressive loss of cortical gray matter in first-episode psychosis, a role for apoptosis in schizophrenia appears plausible. Studies that have examined markers of apoptosis and levels of apoptotic regulatory proteins in postmortem schizophrenia brain tissue will be reviewed in context of this hypothesis. Overall, the data seem to indicate a dysregulation of apoptosis in several cortical regions in schizophrenia, including evidence that the apoptotic vulnerability is increased. Although the exact role of apoptosis in schizophrenia remains uncertain, the potential involvement of non-lethal localized apoptosis is intriguing, especially in earlier stages of the illness.

Apoptosis↗

PubMed2005

Magnetic resonance findings in bipolar disorder.

The MR findings reviewed in this article suggest structural, chemical, and functional abnormalities in specific brain regions participating in mood and cognitive regulation, such as the DLPFC, anterior cingulate, amygdala,STG, and corpus callosum in subjects with bipolar disorder. These abnormalities would represent an altered anterior-limbic network disrupting inter- and intrahemispheric communication and underlying the expression of bipolar disorder. Available studies are limited by several confounding variables, such as small and heterogeneous patient samples, differences in clinical and medication status, and cross-sectional design. It is still unclear whether abnormalities in neurodevelopment or neurodegeneration play a major role in the pathophysiology of bipolar disorder. These processes could act together in a unitary model of the disease, with excessive neuronal pruning/apoptosis during childhood and adolescence being responsible for the onset of the disorder and subsequent neurotoxic mechanisms and impaired neuroplasticity and cellular resilience being responsible for further disease progression. Future MR studies should investigate larger samples of first-episode drug-free patients, pediatric patients, subjects at high risk for bipolar disorder, and unaffected family members longitudinally. Such a study population is crucial to examine systematically whether brain changes are present before the appearance of symptoms (eg, maldevelopment) or whether they develop afterwards, as a result of illness course (eg, neurodegeneration). These studies will also be instrumental in minimizing potentially confounding factors commonly found in adult samples, such as the effects of long-term medication, chronicity, and hospitalizations. Juvenile bipolar patients often have a strong family history of bipolar disorder. Future studies could help elucidate the relevance of brain abnormalities as reflections of genetic susceptibility to the disorder. MR studies associated with genetic, post-mortem, and neuropsychologic studies will be valuable in separating state from trait brain abnormalities and in further characterizing the genetic determinants, the neuropathologic underpinnings, and the cognitive disturbances of bipolar disorder.

Atrophy↗

PubMed2005

No association found between 158 Val/Met polymorphism of the COMT gene and schizophrenia with minor physical anomalies.

The catechol-O-methyl transferase (COMT) gene has been a promising candidate in genetic research on schizophrenia because of its function in dopamine metabolism and its location on chromosome 22q11.2, which may be implicated in both schizophrenia and velocardiofacial syndrome (VCFS). To explore the possible genetic contribution of COMT to the development of schizophrenia, we focused on the subgroup of patients with schizophrenia characterized by minor physical anomalies as a phenotype and the 158 Val/Met polymorphism as a genotype. Since some physical anomalies are found in both schizophrenia and VCFS, schizophrenia patients with minor physical anomalies could represent the putative subgroup of schizophrenia linked to a disruption in neurodevelopment. Genotyping for the 158 Val/Met (472 G>A) polymorphism in the COMT gene was done for 239 patients with schizophrenia and 248 normal controls. Our analysis did not yield any significant between-group differences in terms of either allele or genotype frequency. We also could not find any association between the COMT gene and the schizophrenia subgroup with minor physical anomalies, although there was a significant difference in Waldrop total scores between the patients with schizophrenia and the normal controls. Analyses of subgroups based on other clinical variables also did not reveal significant differences. Overall, this study does not support the hypothesis that the 158 Val/Met polymorphism in the COMT gene is associated with schizophrenia in Koreans.

Adult↗

PubMed2006

Cerebrospinal fluid monoamine metabolite levels in human newborn infants born in winter differ from those born in summer.

An earlier study has shown significant differences in the CSF monoamine metabolite levels in adults born during different seasons of the year. We study here the relationship between season of birth and CSF monoamine metabolite levels in 283 newborn febrile infants without neurological abnormalities, with an age distribution ranging from birth to about 3 months, adjusting for the confounding variables age and time at lumbar puncture, weight at birth, estimated gestational age at birth, gender, race, and medicaid status. Each of the three metabolite levels as well as their ratios HVA/5-HIAA and 5-HIAA/MHPG showed significant month-of-birth variations, but not the ratio HVA/MHPG. For HVA and MHPG levels, the maximum was obtained around the winter birth months November-December, whereas for 5-HIAA level, the maximum was obtained around the summer birth months June-July. The correlations between HVA and 5-HIAA were, in general, significantly positive within the different birth seasons and races. Among summer-born Caucasian infants, MHPG was significantly positively correlated with HVA and with 5-HIAA, whereas among winter-born Black infants, MHPG was significantly positively correlated with HVA. Season of birth is an unspecific environmental factor that may be proxy for several possible seasonally varying environmental circumstances such as the length of photoperiod, temperature, infections, nutrition, stress and lifestyle. Studies relating season of birth to monoaminergic turnover at different stages of life may yield important clues about the gestational and perinatal origins of neurodevelopment.

Female↗

PubMed2005

Fluctuating asymmetry, second to fourth finger length ratios and human sexual orientation.

Sexual orientation in humans may be influenced by levels of prenatal sex steroids which canalise neurodevelopment along sex-typical (heterosexual) or sex-atypical (homosexual) lines. Some evidence for sexual-orientation-related differences in putative somatic markers of prenatal sex hormones supports this view. A competing theory asserts that human homosexuality is due to developmental instability (DI) because it represents a shift from the species-typical pattern of heterosexual orientation. Evidence for elevated rates of non-right handedness among homosexuals provides limited support for this account. The current study tested both theories by examining nine bilateral somatic traits in 120 healthy heterosexual and homosexual men and women in order to compute second to fourth finger length ratios (2D:4D), a measure ascribed to levels of prenatal sex steroids, and fluctuating asymmetry (FA), a measure of DI. Homosexual men and women had significantly lower right hand 2D:4D ratios (even after controlling for handedness, height and weight differences) in comparison to heterosexuals, but sexual orientation did not relate to composite FA scores. The findings constrain the number of possible neurodevelopmental pathways responsible for sexual orientation in humans.

Adult↗

PubMed2006

Stress in pregnancy and infant HPA axis function: conceptual and methodological issues relating to the use of salivary cortisol as an outcome measure.

Problems regulating behaviour and emotions in infancy may be a risk factor for the development of psychopathology later in life. Compelling evidence from animal models suggests that one potential pathway to early dysregulation is fetal programming of the hypothalamic-pituitary-adrenal (HPA) axis. According to this model, prenatal maternal stress and anxiety during sensitive periods of development can lead to enduring changes in fetal and offspring neurodevelopment and behaviour. While there is emerging evidence from human studies to suggest a link between maternal negative mood states in pregnancy and various cognitive, behavioural, and emotional disturbances in offspring, it is not yet clear whether the programming mechanism demonstrated in animal studies also applies to humans. Few studies have directly assessed HPA axis function in the infants of prenatally stressed women. Research in this area has been constrained by a number of measurement challenges unique to the assessment of cortisol in infants. This paper discusses these challenges with a view to stimulating further research in the area.

Animals↗

PubMed2006

The need for developmental neurotoxicity studies in risk assessment for developmental toxicity.

The estimated frequencies of neurodevelopmental disorders in children are relatively high, i.e. around 12%. The developing central nervous system appears to be especially susceptible to toxic insults and several developmental neurotoxicants, some with widespread occupational or consumer exposure, have been identified in humans and experimental animals. Cross-species comparability between human and experimental animals supports the assumption that developmental neurotoxicity (DNT) effects in animals indicate a potential to affect development in humans. The proposed Organization for Economic Cooperation and Development (OECD) developmental neurotoxicity study (TG 426) provides an outline of behavioural and morphological endpoints that are relevant to human neurodevelopment, and the guideline is expectedly adopted during 2006. Hopefully, this may contribute to inclusion of sufficient regulatory testing for DNT in the new EU chemical regulation REACH (Registration, Evaluation, Authorisation and Restriction of Chemicals). At present, DNT testing is not included in REACH and that gives rise to concern, as there is a recognized need for DNT testing in order to protect the susceptible developing brain.

Animals↗

PubMed2004

GSK-3 parameters in postmortem frontal cortex and hippocampus of schizophrenic patients.

The protein kinase glycogen synthase kinase-3 (GSK-3) is highly abundant in brain and involved in signal transduction cascades, particularly during neurodevelopment. We have previously found reduced GSK-3beta mRNA levels, protein levels and GSK-3 total (alpha+beta isoforms) activity in postmortem frontal cortex of schizophrenic patients in the Stanley Medical Research Institute's Brain Collection. To verify and extend these findings, GSK-3 parameters were now measured in the frontal cortex (BA9) and hippocampus obtained from the Rebecca L. Cooper Research Laboratories postmortem brain collection. Fifteen pairs of schizophrenic patients and matched control subjects have been studied. No significant differences in GSK-3alpha and GSK-3beta mRNA levels, GSK-3beta protein levels or total GSK-3 (alpha+beta) activity were found in the frontal cortex of the two diagnostic groups. Hippocampal GSK-3alpha and GSK-3beta mRNA levels were significantly lower (22% and 28%, respectively) in the tissue from the schizophrenic patients compared with the normal controls. Hippocampal GSK-3beta protein levels in the schizophrenic patients were 24% significantly lower than control values only after omission of three outlier subjects. Hippocampal total GSK-3 (alpha+beta) activity in the patients was 31% lower in the schizophrenic patients vs. control subjects. This difference was marginally significant. While our previous data on GSK-3beta in postmortem brain and the recent report that there is impaired AKT1-GSK-3beta signaling in schizophrenia suggest that changes in pathways involving protein kinases such as AKT1 and GSK-3beta in schizophrenia are complex, our present data do not provide strong evidence in support of the involvement of GSK-3beta in schizophrenia. Therefore, further investigation in a greater number of brain samples is warranted to better clarify the possible role of this enzyme in the pathophysiology of schizophrenia.

Enzyme-Linked Immunosorbent Assay↗

PubMed2004

A developmental model for similarities and dissimilarities between schizophrenia and bipolar disorder.

Schizophrenia and mania have a number of symptoms and epidemiological characteristics in common, and both respond to dopamine blockade. Family, twin and molecular genetic studies suggest that the reason for these similarities may be that the two conditions share certain susceptibility genes. On the other hand, individuals with schizophrenia have more obvious brain structural and neuropsychological abnormalities than those with bipolar disorder; and pre-schizophrenic children are characterised by cognitive and neuromotor impairments, which are not shared by children who later develop bipolar disorder. Furthermore, the risk-increasing effect of obstetric complications has been demonstrated for schizophrenia but not for bipolar disorder. Perinatal complications such as hypoxia are known to result in smaller volume of the amygdala and hippocampus, which have been frequently reported to be reduced in schizophrenia; familial predisposition to schizophrenia is also associated with decreased volume of these structures. We suggest a model to explain the similarities and differences between the disorders and propose that, on a background of shared genetic predisposition to psychosis, schizophrenia, but not bipolar disorder, is subject to additional genes or early insults, which impair neurodevelopment, especially of the medial temporal lobe.

Amygdala↗

PubMed2005

Cumulative exposure to estrogen and psychosis: a peak bone mass, case-control study in first-episode psychosis.

The organizational structural effects of estrogen may be cumulative and permanent by impacting on neurodevelopment, giving rise to "neuroprotective" effects and eventually reduction of psychosis risk. Reduction in bone mineral density (BMD, in g/cm2), as a biological marker of reduced cumulative exposure to estrogen, may be a marker of increased psychosis risk. A sample of 19 first-episode female psychosis patients with minimal previous antipsychotic exposure (mean 10 weeks) and 20 female controls underwent advanced fan-beam dual X-ray absorptiometry (DXA) to assess lumbal spine BMD of the region of L1-L4. Mean BMD was around one standard deviation lower in patients (1.13, S.D.=0.10) than in controls (1.25, S.D.=0.12; p=0.0021), and 84% of patients scored below the median value of the controls (OR=5.3, 95% CI: 1.2, 24.2). The results are compatible with the hypothesis that psychosis in women may be associated causally with a reduced protective effect of estrogen over the course of development.

Absorptiometry, Photon↗

PubMed2005

Genetic and post-mortem mRNA analysis of the 14-3-3 genes that encode phosphoserine/threonine-binding regulatory proteins in schizophrenia and bipolar disorder.

BACKGROUND: Previous work with animal models of psychosis, human genetic studies, and human post-mortem gene expression studies implicate the 14-3-3 family of genes in schizophrenia. The 14-3-3 genes code for a family of proteins that bind to and regulate other proteins, and they modulate neurodevelopment, cell-division, signal transduction and gene transcription. OBJECTIVE: To explore the role of five 14-3-3 isoforms (beta, gamma, epsilon, zeta, and eta) in schizophrenia by: (1) comparing mRNA levels in post-mortem brain from schizophrenic, bipolar and control subjects and (2) assessing genetic association with schizophrenia in both case-control and nuclear family samples. METHODS: Quantitative PCR (q-PCR) was used to determine relative mRNA levels in dorsolateral prefrontal cortex (Brodmann's area 46) samples donated by the Stanley Medical Research Institute (SMRI). Selected SNPs were genotyped in all five isoforms for association analysis in both family and case-control samples. RESULTS: No significant differences in 14-3-3 mRNA expression levels between the diagnostic groups were found. A significant genetic association with schizophrenia was found for the 14-3-3zeta isoform in a subset of nuclear families of British ancestry (TDT: chi(2)=7.2; df=1; p=0.0073), in the case-control sample overall (p=0.011), and in a subset of the case-control sample. CONCLUSION: The results, in combination with other published evidence, suggest that further work is necessary to clarify what role the 14-3-3 genes may play in the etiology and pathogenesis of schizophrenia.

14-3-3 Proteins↗

PubMed2005

Infant motor development and adult cognitive functions in schizophrenia.

BACKGROUND: Childhood neuromotor dysfunction is a risk factor for schizophrenia, a disorder in which cognitive deficits are prominent. The relationship between early neurodevelopment and adult cognition in schizophrenia remains unclear. METHODS: We examined the associations between infant motor development and adult cognitive functions in schizophrenia (n = 61) and the general population (n = 104) in a sample drawn from the The Northern Finland 1966 Birth Cohort. Data on ages of learning to stand and walk with or without support were obtained at age 12 months by health visitor assessment. Neurocognitive measures at age 33-35 included executive function, verbal and visual episodic memory, and visuo-spatial working memory. RESULTS: The schizophrenia group achieved neuromotor milestones later and performed significantly worse than the control group on all measures of cognition. In pooled analyses there were associations between infant motor development and adult cognition in the domains of executive function, verbal learning and visuospatial working memory, but not in visual object learning. The pattern of associations between development and cognition was similar in schizophrenia and the general population. CONCLUSIONS: These findings are consistent with the hypothesis that in schizophrenia mild infant motor developmental delay and adult cognitive deficits (at least in some domains) are age dependent manifestations of the same underlying neural process. Thus, they may be better considered as part of a single longitudinal syndrome.

Adult↗

PubMed2006

Gene regulation by hypoxia and the neurodevelopmental origin of schizophrenia.

Neurodevelopmental changes may underlie the brain dysfunction seen in schizophrenia. While advances have been made in our understanding of the genetics of schizophrenia, little is known about how non-genetic factors interact with genes for schizophrenia. The present analysis of genes potentially associated with schizophrenia is based on the observation that hypoxia prevails in the embryonic and fetal brain, and that interactions between neuronal genes, molecular regulators of hypoxia, such as hypoxia-inducible factor 1 (HIF-1), and intrinsic hypoxia occur in the developing brain and may create the conditions for complex changes in neurodevelopment. Consequently, we searched the literature for currently hypothesized candidate genes for susceptibility to schizophrenia that may be subject to ischemia-hypoxia regulation and/or associated with vascular expression. Genes were considered when at least two independent reports of a significant association with schizophrenia had appeared in the literature. The analysis showed that more than 50% of these genes, particularly AKT1, BDNF, CAPON, CCKAR, CHRNA7, CNR1, COMT, DNTBP1, GAD1, GRM3, IL10, MLC1, NOTCH4, NRG1, NR4A2/NURR1, PRODH, RELN, RGS4, RTN4/NOGO and TNF, are subject to regulation by hypoxia and/or are expressed in the vasculature. Future studies of genes proposed as candidates for susceptibility to schizophrenia should include their possible regulation by physiological or pathological hypoxia during development as well as their potential role in cerebral vascular function.

Animals↗

PubMed2006

No evidence for an association between the BDNF Val66Met polymorphism and schizophrenia or personality traits.

Brain-derived neurotrophic factor (BDNF) is a member of the nerve growth factor family, which plays a critical role in neurodevelopment. Based on the neurodevelopmental hypothesis, the BDNF gene has been a candidate locus for schizophrenia. In Caucasians, recent studies identified an association with the Val66Met polymorphism, which has been suggested to affect episodic memory and hippocampal function in humans. However, in other populations, the association has not been replicated. In the present study, we investigated the association between the Val66Met polymorphism of the gene and schizophrenia in 401 Japanese patients with schizophrenia and 569 controls. As a result, we did not observe a significant difference in genotypic distribution or allele frequencies between the patients and controls (chi2=0.56, df=2, p=0.76 and chi2=0.39, df=1, p=0.53, respectively). We also investigated the association between the polymorphism and personality traits in the controls; however, no significant association was observed. Thus, the present study did not provide evidence for an association between the BDNF gene and schizophrenia or personality traits in the Japanese population.

Asian People↗