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PubMed1996

Morphometric and neurodevelopmental outcome at age five years of the offspring of women who continued to exercise regularly throughout pregnancy.

OBJECTIVE: To test the hypothesis that continuing regular, vigorous, sustained exercise throughout pregnancy adversely affects morphometric and neurodevelopmental outcome in offspring at 5 years of age. STUDY DESIGN: The offspring of 20 women who exercised were compared with those of 20 physically active control subjects. The women and their offspring were matched for multiple prenatal and postnatal variables known to influence outcome. All women were enrolled before the index pregnancy, monitored throughout, and had clinically normal antenatal, intrapartum, and postnatal courses. Morphometric measures were obtained at birth and at 5 years of age by a single, trained observer. Neurodevelopment was assessed by developmental psychologists masked to maternal exercise status. Data were analyzed with an unpaired Student t test. RESULTS: At birth, head circumference and length were similar, but the offspring of the exercising women weighed less (3.40 +/- 0.80 vs 3.64 +/- 0.70 kg) and had less fat (10.5% +/- 0.9% vs 15.1% +/- 0.6%). At 5 years of age, head circumference and height were similar, but the offspring of the women who exercised weighed less (18.0 +/- 0.5 vs 19.5 +/- 0.6 kg) and had a lower sum (sigma) of five site skinfolds (37 +/- 1 vs 44 +/- 2 mm). Motor, integrative, and academic readiness skills were similar. However, the exercise offspring performed significantly better on the Wechsler scales (125 +/- 2 vs 116 +/- 3) and tests of oral language skills (119 +/- 2 vs 109 +/- 3). CONCLUSIONS: These data refute the hypothesis and suggest that exercise during pregnancy reduces the subcutaneous fat mass of the offspring.

Adult↗

PubMedDate not supplied

Relationship between impairment of prenatal brain growth and family history of psychosis in schizophrenia.

Recently McNeil et al. (1993b), showed that schizophrenics had smaller head circumference (HC) at birth than controls. This small head size at birth was observed more commonly among schizophrenics without a family history of psychosis than among familial schizophrenics, suggesting that some prenatal environmental factors, rather than genetic factors, are related to the impaired brain growth in utero. We attempted to replicate this finding in 100 Japanese schizophrenics (DSM-III-R), using contemporaneous data on body measures at birth. Conversely, in the current study, HC at birth was found to be significantly smaller in schizophrenics with a family history of psychosis (N = 19) than those without (N = 81). A multiple regression analysis, controlling for gender, gestational age, maternal age, birth order and year of birth, yielded an overall reduction of about 1 cm in HC at birth among familial schizophrenics compared with non-familial schizophrenics. When HC at birth in family history positive and negative groups was compared separately with the local population norms with adjustment for gender and gestational age, familial and non-familial schizophrenics were both found to have significantly smaller HC at birth, although the difference was less marked for the latter. These results suggest that schizophrenics have delayed cerebral development in utero, and that genes which operate on prenatal neurodevelopment may play an important role in the aetiology of schizophrenia, although it is possible that some environmental factors may also be involved in the impaired brain growth.

Adult↗

PubMedDate not supplied

Neuropathological studies of brain tissue in schizophrenia.

Postmortem neuropathological investigations in the last half decade provide increasing evidence compatible with a neurodevelopmental defect in schizophrenia. Basic and clinical data support hypotheses suggesting that disturbances in neurodevelopment in schizophrenia may involve the cortical subplate and a theorized second trimester "window of vulnerability". The focus of this paper is on (1) selected methodological issues involved in the collection, analyses and preservation of human postmortem brain tissue; (2) a review of evidence showing morphological defects particularly in prefrontal cortical regions of the schizophrenic brain; and (3) potential future research directions.

Brain↗

PubMedDate not supplied

Which characteristics of schizophrenia predate psychosis?

Neuropsychological and brain structural abnormalities are present in first onset schizophrenia; the balance of evidence is that in the majority of cases these are developmental in origin. A proportion of first degree relatives also show lateral ventricular enlargement, cortical volume decrease and possibly loss of the normal cerebral asymmetry; these findings suggest that certain families transmit a genetic defect in the control of neurodevelopment. On the contrary, decrement in left hippocampal volume appears to be secondary to perinatal hypoxia. High risk, follow-back and cohort studies all demonstrate that preschizophrenics as a group show deviant development; delayed milestones, lower IQ, solitary play, excessive anxiety, and minor neurological problems are all common. It seems likely, but not proven, that these are a manifestation of underlying neurodevelopmental disorder.

Adolescent↗

PubMedDate not supplied

Regional brain volume change over the life-time course of schizophrenia.

The concept that schizophrenia has its antecedents in neurodevelopment has long been debated and has been at the forefront of research on this disorder over the last decade. However new recent evidence from controlled longitudinal studies indicates that some of the structural brain anomalies observed in schizophrenia may continue to progress sporadically after the onset of clinical illness. The studies vary in cohort composition, stage of illness studied, duration of follow-up interval, and specific brain regions with findings. Nevertheless, the findings as a whole suggest that the brain changes in size throughout the lifespan of an individual and to a greater extent in schizophrenia. While the detected abnormalities could be explained by various technical artifacts, or physiological epi-phenomena, that they result from an ongoing neurochemical, physiological or morphological process characteristic of the underlying basis for the disorder is an intriguing possibility that lends itself to possible future intervention.

Aging↗

PubMed2002

Schizophrenia-like illness in velo-cardio-facial syndrome: a genetic subsyndrome of schizophrenia?

BACKGROUND: The study of genetic illnesses that have a behavioral phenotype resembling psychosis can provide important insights into the genetic basis of psychotic disorders and their patho-mechanisms. An important example of such a genetic disorder is the velo-cardio-facial syndrome (VCFS) associated with 22q11 microdeletion. CASE REPORT: The case of a 22-year-old male, who had the typical genotype and phenotype of VCFS and developed a psychotic illness characterized by withdrawal, catatonic posturing, inappropriate affect, stereotyped behavior, negativism and poverty of speech, is described. He had a partial response to an atypical neuroleptic, but developed myoclonus that was controlled with an anticonvulsant. CONCLUSION: The association of VCFS with schizophrenia-like psychosis is worthy of further study as it may provide insights into the molecular basis of neurodevelopment and its aberrations in psychotic disorders.

Abnormalities, Multiple↗

PubMed2003

Psychosocial adaptation after solid organ transplantation in children.

The possibility of extending life with advanced medical procedures such as organ transplantation in childhood has made it possible to focus on patients' well-being in a wider perspective. They still experience a high prevalence of medical and physical disabilities, which definitively have an impact on a child's psychosocial adjustment after transplantation. Many disabilities originate before transplantation, and much effort should be taken to diminish possible complications and ameliorate growth and neurodevelopment, which have an impact for later adjustment regardless of a successful transplantation. Well-being and QOL are not necessarily always correlated to the degree of physical disability. Different social, financial, and demographic factors also have an impact, as do children's and families' ability to cope with a chronic disorder. Nonadherence and noncompliance are a great problem, particularly in adolescents. They are the result and a possible cause of inferior psychosocial adjustment. Continuous multidisciplinary support, follow-up, and education are needed to cope with this problem. Validated and reliable health status measures in pediatric transplant recipients are scarce in the literature, and few assessments can be completed by the children themselves. A continuing effort must be made to improve psychosocial adjustment and QOL after transplantation to achieve the ultimate goal in medicine: the overall well-being of our patients.

Adaptation, Psychological↗

PubMed2001

Pesticides in children.

Children are exposed to a wide range of pesticides, including insecticides, herbicides, fungicides, and rodenticides. They differ from adults in their exposures and responses to exposures. Acute and chronic toxicity are discussed, and important chronic effects, such as carcinogenesis, endocrine disruption, and neurodevelopment effects are reviewed. The state of laws and regulations are also discussed. Recommendations are made to pediatricians regarding treatment and advising families regarding avoidance of pesticide exposures and their effects.

Child↗

PubMed1993

Learning disabilities.

Although the major manifestations of learning disabilities are expressed in the classroom, the pediatrician has several important roles to play. Identification may be achieved in the early school years by systematic observation of the child's neurodevelopment and school progress. Confirmation of the diagnosis is the most commonly assumed role. Interpretation and explanation of learning disabilities to the parents and child follow. The goals of treatment of learning disabilities are achievement of academic competence, treatment of associated deficits, and prevention of adverse mental health outcomes. The long-term relationship between the family and pediatrician facilitates the performance of longitudinal monitoring to ensure that the program is accomplishing its goals and that outcome is optimal.

Adolescent↗

PubMed1996

Neurodevelopmental outcome at age two years amongst very low birth weight infants: results from a district general hospital.

STUDY OBJECTIVES: To describe the survival and neurodevelopmental outcome at age 2 years of very low birth weight infants from routinely collected information in a district general hospital setting. DESIGN: Case note review and child health surveillance information was collected on all liveborn < 1,501 g infants born in our district general hospital over 4 years, 1989-1992. Main outcome measures were (a) death before discharge, (b) normal neurodevelopment at age 2 years, (c) minor impairment at age 2 years, (d) major impairment at age 2 years. Comparability with other published work was examined. SETTING: Rotherham District General Hospital, a maternity unit with neonatal intensive care facilities. Selected infants were transferred for continuing neonatal intensive care to a tertiary unit. Most infants were followed up to age 2 years in a dedicated clinic. SUBJECTS: Liveborn very low birth weight infants. MAIN RESULTS: Over the 4 year period there were 125 liveborn infants < 1,501 g; 93 (74%) survived to discharge home. Defined neurodevelopmental outcome measures were easily retrievable in 92 children at age 2 years from hospital case notes or child health surveillance records. Sixty-four children (70%) were neurodevelopmentally normal, 10 children (11%) had a major impairment (mostly cerebral palsy) and 18 (19%) had an isolated minor impairment. CONCLUSIONS: The incidence of major impairment amongst very low birth weight infants in our district general unit is broadly comparable with other published series. Outcome measures of neurodevelopmental status are available from routinely collected clinical information. The use of such measures to make detailed comparisons between units is problematical because of a wide range of confounding variables.

Child, Preschool↗

PubMed2004

Membrane phospholipids and cytokine interaction in schizophrenia.

Although the potential key role that lipids may have in schizophrenia is not fully understood, multiple lines of evidence to date implicate the lipid environment in the behavior of neurotransmitter systems. Decreased phospholipid polyunsaturated fatty acids (PUFAs) have been demonstrated in both brain and peripheral membranes in schizophrenia, which is consistent with the hypothesis of myelin-related dysfunction in schizophrenia. Membrane defects, such as those induced by decreased PUFAs in phospholipids, can significantly alter a broad range of membrane functions and ipso facto behavior through multiple "downstream" effects. A number of putative mechanisms have been identified to explain the decreased PUFAs in schizophrenia, notably the increased turnover of phospholipids and decreased incorporation of arachidonic acid (AA) in membranes. In addition to increased oxidative stress, altered immune function may also be responsible for increased phospholipase activities. This association is particularly relevant in relation to phospholipids/PUFA, as AA can be converted to a variety of biologically active compounds, such as eicosanoids, which serve as potent messengers in regulating the inflammatory response, as well as endocannabinoids, which may affect schizophrenic psychopathology. Direct evidence of immune changes in some patients with schizophrenia have come to light, particularly in the activities of several cytokines known to be altered in autoimmune dysfunction. Given the diverse physiological function of AA, the specific behavioral symptomatology of schizophrenia is related mostly to the effect of AA changes that regulates neurodevelopment, neurotransmitter homeostasis, phosphatidylinositol signaling, and neuromodulatory actions of endocannabinoids in schizophrenia. Hence, in the current conceptualization, AA may be at a nexus point in the cascade leading to the syndrome of schizophrenia and represents a common biochemical pathway leading to the varied symptomatology of this disorder.

Animals↗

PubMed2004

S100B in schizophrenic psychosis.

Recent findings have strengthened the hypothesis that a dysfunction of neuronal synapses and dendrites is relevant for the pathogenesis of schizophrenia. It might be present during neurodevelopment as well as in degenerative and regenerative processes of the mature brain. S1OOB, a small, Ca2+-binding, astrocytic protein, plays an important role in modulating the proliferation and differentiation of neurons and glia cells. It is involved in the regulation of cellular energy metabolism and interacts with many immunological functions of the brain. This review addresses findings from cell cultural and animal experiments potentially pertinent for the pathogenesis of schizophrenic psychoses. Morphological and functional data are analyzed and clinical studies reporting alterations of S1OOB concentrations in schizophrenic patients are reviewed. Evidence and limitations of the available studies are pointed out and promising future research strategies are outlined.

Animals↗

PubMed1992

Neurotransmitters as neurotrophic factors: a new set of functions.

At the start of this review, factors were deemed trophic if they stimulated mitosis, permitted neural cell survival, promoted neurite sprouting and growth cone motility, or turned on a specific neuronal phenotype. The in vitro evidence from cell cultures is overwhelming that both neurotransmitters and neuropeptides can have such actions. Furthermore, the same chemical can exert several of these effects, either on the same or on different cell populations. Perhaps the most striking example is that of VIP, which can stimulate not only mitosis, but also survival and neurite sprouting of sympathetic ganglion neuroblasts (Pincus et al., 1990a,b). The in vivo data to support the in vitro experiments are starting to appear. A role for VIP in neurodevelopment is supported by in vivo studies that show behavioral deficits produced in neonatal rats by treatment with a VIP antagonist (Hill et al., 1991). The work of Shatz' laboratory (Chun et al., 1987; Ghosh et al., 1990) suggests that neuropeptide-containing neurons, transiently present, serve as guideposts for thalamocortical axons coming in to innervate specific cortical areas. Along similar lines, Wolff et al. (1979) demonstrated gamma-aminobutyric acid-accumulating glia in embryonic cortex that appeared to form axoglial synapses and suggested the possibility that gamma-aminobutyric acid released from the glia might play a role in synaptogenesis by increasing the number of postsynaptic thickenings. Meshul et al. (1987) have provided evidence that astrocytes can regulate synaptic density in the developing cerebellum. The work of Zagon and McLaughlin (1986a,b, 1987) has shown that naltrexone, an antagonist of the endogenous opioid peptides, affects both cell number and neuronal sprouting. Lauder's laboratory (Lauder et al., 1982) has shown a role for 5-HT in regulation of the proliferation of numerous cell types. These studies illustrate another important point, that neurotransmitters and neuropeptides function in communication not only between neurons, but also between neurons and glial cells, and between glial cells. Given that astrocytes can express virtually all of the neural receptors and can produce at least some of the neurotransmitters and neuropeptides, they must now be considered equal partners in the processes of intercellular communication in the nervous system, including the trophic responses. The actions of neurotransmitters and neuropeptides have to be considered in terms of a broad spectrum of actions that range from the trophic actions described in this review, to the classic transmitter actions, to potential roles in neurotoxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2005

Sexual dimorphism in cerebellar structure, function, and response to environmental perturbations.

Sexual dimorphism of CNS structure and function has been observed in humans and animals, but remains relatively unrecognized in the context of the cerebellum. Recent research in our laboratory has examined whether these gender differences extend to cerebellar structure and function, as well as the impact of environmental factors on the developing cerebellum. Perinatal exposure to both chemical and physical perturbations in the environment (in our experiments, PCBs or hypergravity) affects growth, neurodevelopment, and motor coordination differently in males and females. These neurodevelopmental and behavioral effects are accompanied by sex-related changes in cerebellar mass and cerebellar protein expression. Exposure to chemical toxins (PCBs) resulted in more dramatic neurodevelopmental and behavioral changes in male neonates. It is possible that gender-related differences in male and female cerebellar structure and function are related to sex-specific development of the cerebellum and sex-specific distribution of specific receptors, local synthesis of trophic factors, and maturation of the pituitary hypophesial axis. These sex-related differences may underlie the sex-specific preponderance of certain neuropsychiatric disorders, and must be incorporated in the design of future basic and clinical investigations.

Animals↗

PubMed1998

Nitric oxide in neurodegeneration.

Nitric oxide (NO) is a unique biological messenger molecule which mediates diverse physiologic roles. NO mediates blood vessel relaxation by endothelium, immune activity of macrophages and neurotransmission of central and peripheral neurons. NO is produced from three NO Synthase (NOS) isoforms: Neuronal NOS (nNOS), endothelial NOS, and inducible NOS (iNOS). In the central nervous system, NO may play important roles in neurotransmitter release, neurotransmitter reuptake, neurodevelopment, synaptic plasticity, and regulation of gene expression. However, excessive production of NO following a pathologic insult can lead to neurotoxicity. NO plays a role in mediating neurotoxicity associated with a variety of neurologic disorders, including stroke, Parkinson's Disease, and HIV dementia.

AIDS Dementia Complex↗

PubMed2002

Neurobehavioral development of two mouse lines commonly used in transgenic studies.

The present study was aimed at establishing the differences in the neurodevelopmental profile between two F2 lines derived from two F1 hybrid mouse strains (129 x C57BL/6 and C57BL/6 x SJL). The choice of the given strains was based on the frequent use of these mice in transgenic research. For the neurodevelopment phenotyping, we employed a test battery consisting of 23 somatometric, sensorial and motor tests. Significant variations between the strains were established in different functional domains. Some specific delays in the appearance of developmental landmarks were observed in F2 mice derived from crosses of F1 C57BL/6 x 129, whereas they acquired early developmental functions, such as the righting reflex, sooner than C57BL/6 x SJL-derived mice. C57BL/6 x 129 F2 offspring were spontaneously hypoactive, and their poorer motor performance was confirmed by low performance in the negative geotaxis test. However, there were no differences in the general psychomotor development as shown by the good performance in the homing test in both F2 lines. Both strains were susceptible to the handling procedures used, presenting a similar alteration in the response observed in the homing test as compared to nonhandled control mice. In conclusion, our work highlights the importance of the genetic background for transgenesis experiments and also the need for well-established testing protocols to obtain sufficient information at the first stage of behavioral screening of genetically modified mice.

Animals↗

PubMed1997

Neuropilin is a semaphorin III receptor.

The semaphorin family contains a large number of phylogenetically conserved proteins and includes several members that have been shown to function in repulsive axon guidance. Semaphorin III (Sema III) is a secreted protein that in vitro causes neuronal growth cone collapse and chemorepulsion of neurites, and in vivo is required for correct sensory afferent innervation and other aspects of development. The mechanism of Sema III function, however, is unknown. Here, we report that neuropilin, a type I transmembrane protein implicated in aspects of neurodevelopment, is a Sema III receptor. We also describe the identification of neuropilin-2, a related neuropilin family member, and show that neuropilin and neuropilin-2 are expressed in overlapping, yet distinct, populations of neurons in the rat embryonic nervous system.

Amino Acid Sequence↗

PubMed2002

Lipids with an emphasis on long-chain polyunsaturated fatty acids.

In addition to their role as a source of energy, several fatty acids are important components of cell membranes and/or precursors of biologically important eicosanoids. The long-chain polyunsaturated fatty acids, docosahexaenoic acid (DHA) and arachidonic acid (AA), are important for optimal visual function and neurodevelopment. These fatty acids are present in human milk but, until recently, have not been included in formulas marketed in the United States. Although the results of clinical trials assessing the effect of DHA and AA intakes on visual and cognitive development have been inconsistent, some studies suggest benefits. Adequate intake of these fatty acids may be especially important for the preterm infant.

Animals↗