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PROTECTING THE PRETERM FETAL BRAIN FROM HYPOXIA AND INFECTION: A HEALTHY START TO LIFE.
Funder
National Health and Medical Research Council
Funding Amount
$495,750.00
Summary
Brain damage during fetal life is a significant cause of later neurological problems such as cerebral palsy. Recent studies have shown that brain injury detected in infants is usually caused by adverse conditions within the uterus prior to labour, but the exact causes are poorly understood. It is also apparent that babies born prematurely are at increased risk of suffering serious brain damage. In recent years it has become evident that infections in the mother may be linked to both premature bi ....Brain damage during fetal life is a significant cause of later neurological problems such as cerebral palsy. Recent studies have shown that brain injury detected in infants is usually caused by adverse conditions within the uterus prior to labour, but the exact causes are poorly understood. It is also apparent that babies born prematurely are at increased risk of suffering serious brain damage. In recent years it has become evident that infections in the mother may be linked to both premature birth and brain damage. It has been proposed that certain chemicals (cytokines), which are released during an infection, can cross the placenta to the fetus causing inflammatory changes that lead to brain damage. We have shown that an inflammatory inducing chemical (bacterial endotoxin) administered to immature fetal sheep induces brain damage similar to that seen in cerebral palsy. This provides an excellent model for testing agents that are known to block the action of cytokines and other markers of inflammation; currently there is no effective strategy for the treatment or prevention of hypoxia and inflammatory induced injury of the brain partly due to our ignorance about how and when the damage is occurring. We will test the effects of two chemicals; N-acetyl cysteine, which is known to block the generation of inflammatory cytokines, and the naturally occurring glycoprotein erythropoietin, which prevents death of neurons (apoptosis). We hope that by blocking these pathways we may be able to prevent brain injury from occurring when the immature fetus is exposed to an infection during gestation. We expect that this project will provide important novel information that helps us to understand how infection in the mother can cause brain injury in the fetus and provide a new approach for strategies to prevent or treat brain injury.Read moreRead less
Molecular And Cellular Mechanisms Of Axon Guidance In The Vertebrate Nervous System
Funder
National Health and Medical Research Council
Funding Amount
$330,735.00
Summary
There are, at least, two major obstacles that have to be overcome in the design of therapies to assist the repair of injured brain tissue. First, the nerve cells that are damaged have to be encouraged to regrow - typically this regrowth is inhibited in the brain; and second, this regrowth has to be directed so that the correct connections are re-established. This project will begin to unravel some of the mechanisms that nerve cells use to wire up together during development. This information can ....There are, at least, two major obstacles that have to be overcome in the design of therapies to assist the repair of injured brain tissue. First, the nerve cells that are damaged have to be encouraged to regrow - typically this regrowth is inhibited in the brain; and second, this regrowth has to be directed so that the correct connections are re-established. This project will begin to unravel some of the mechanisms that nerve cells use to wire up together during development. This information can be used to assist in trying to modulate and facilitate directed regrowth following injury.Read moreRead less
INVESTIGATING THE VALIDITY OF PRENATAL INSULTS AS RISK FACTORS FOR SCHIZOPHRENIA.
Funder
National Health and Medical Research Council
Funding Amount
$201,100.00
Summary
Schizophrenia is one of the most devastating of human mental disorders affecting about 1% of the population. The cause of this disorder is not known but it seems certain that it will involve genetic and environmental factors. An adverse environmental factor could be a reduced supply of oxygen and nutrients to a baby during pregnancy. In guinea pigs we aim to investigate whether disruption to the normal supply of oxygen and nutrients to the fetus disrupts the normal fine structure and chemical ma ....Schizophrenia is one of the most devastating of human mental disorders affecting about 1% of the population. The cause of this disorder is not known but it seems certain that it will involve genetic and environmental factors. An adverse environmental factor could be a reduced supply of oxygen and nutrients to a baby during pregnancy. In guinea pigs we aim to investigate whether disruption to the normal supply of oxygen and nutrients to the fetus disrupts the normal fine structure and chemical make up of the brain and gives rise to long-lasting structural and neurochemical changes in adolescent animals, which resemble changes found in the brains of patients with schizophrenia. We will also assess whether behavioural responses of compromised animals are altered in tests that parallel disturbances seen in patients with schizophrenia. Such abnormal brain development could create an underlying vulnerability in the brain, predisposing individuals with risk factors such as genetic inheritance to develop the symptoms of schizophrenia in later life perhaps only after the complete formation of nerve pathways involved in higher brain functioning. If guinea pigs that have been subjected to low oxygen levels during pregnancy show sustained changes in the structure and neurochemistry in regions of the brain that are altered in patients with schizophrenia it would suggest that these long lasting disturbances could result from problems during pregnancy. Thus, this would support the idea that abnormal brain development during pregnancy is one of the underlying causes of schizophrenia.Read moreRead less
FETAL BRAIN INJURY RESULTING FROM INTRAUTERINE INFECTION: LONG TERM CONSEQUENCES AND THE POTENTIAL FOR INTERVENTION
Funder
National Health and Medical Research Council
Funding Amount
$452,640.00
Summary
Brain damage during fetal life is a significant cause of later neurological problems such as cerebral palsy. Recent studies have shown that brain injury detected in infants is usually caused by adverse conditions within the uterus prior to labour, but the exact causes are poorly understood. It is also apparent that babies born prematurely are at increased risk of suffering serious brain damage. Unfortunately, at present, it is not possible to prevent or effectively treat brain damage in the fetu ....Brain damage during fetal life is a significant cause of later neurological problems such as cerebral palsy. Recent studies have shown that brain injury detected in infants is usually caused by adverse conditions within the uterus prior to labour, but the exact causes are poorly understood. It is also apparent that babies born prematurely are at increased risk of suffering serious brain damage. Unfortunately, at present, it is not possible to prevent or effectively treat brain damage in the fetus or newborn, partly due to ignorance about how and when the damage is occurring. In recent years it has become evident that infections in the mother, may be linked to both premature birth and brain damage. It has been proposed that the certain chemicals (cytokines) which are released during an infection can across the placenta to the fetus, causing inflammatory changes that lead to brain damage. However, although associations have been shown in studies of women, there is little evidence that infections actually cause brain damage in the fetus. This project will define the effects of an inflammation inducing chemical (bacterial endotoxin) on the fetal brain and the pattern of inflammation it sets up in the fetus. We will also examine the effects of brain damage caused by endotoxin in the newborn lamb, and relate this to alterations in behaviour. Once we have defined the effects of endotoxin on brain structure, we will test the effects of chemicals that are known to block the actions of inflammatory cytokines. We hope that by blocking the chemical pathway that leads to the production of harmful cytokines we may be able to prevent brain injury from occurring when the fetus is exposed to an infection in the mother. It is expected that this project will provide important information that helps us to understand how infection in the mother can cause brain injury in the fetus. This information is vital if strategies to prevent or treat brain injury are to be developed.Read moreRead less
Compromised Fetal Brain Development: Neurogenesis And The Potential For Therapeutic Intervention.
Funder
National Health and Medical Research Council
Funding Amount
$497,280.00
Summary
Lack of oxygen to the fetal brain during pregnancy is thought to be the main causes of brain injury in newborns. Some of these infants will suffer developmental and behavioural problems including cerebral palsy, schizophrenia and epilepsy. Currently, there is no effective treatment to redress these changes in brain development and this is one of the major challenges in perinatal medicine today. We have previously shown in a guinea pig model of chronic placental insufficiency (reduced oxygen and ....Lack of oxygen to the fetal brain during pregnancy is thought to be the main causes of brain injury in newborns. Some of these infants will suffer developmental and behavioural problems including cerebral palsy, schizophrenia and epilepsy. Currently, there is no effective treatment to redress these changes in brain development and this is one of the major challenges in perinatal medicine today. We have previously shown in a guinea pig model of chronic placental insufficiency (reduced oxygen and nutrient levels during pregnancy) that there is a reduction in neurons and in the connections between them. This may result from a reduction in number of newly generated neurons (neurogenesis), or an increase in neuronal death (apoptosis), or both. To develop therapeutic strategies to improve brain growth and ultimately functional recovery, we must understand the mechanisms which lead to these brain changes. In this project, we will use our guinea pig model to: 1) determine whether a suboptimal fetal environment decreases neuronal numbers by influencing neurogenesis, apoptosis or both, 2) study changes in the compromised brain environment which are likely to influence apoptosis and neurogenesis, 3) determine whether a suboptimal fetal environment has long-term effects on adult neurogenesis and 4) determine whether treatment with erythropoietin (Epo), a naturally occurring hormone, can resolve deficits in brain development and function. Epo is an exciting candidate as it is, or is in the process of being used to treat stroke and newborn asphyxiation. Epo has also been shown to prevent neuronal death and promote neurogenesis following brain injury. Understanding the mechanisms and finding effective treatments for brain damage is a vital area of endeavour if we are to help infants develop their maximum potential and reduce the enormous social, economic and educational burden which must be borne by the individual and society in general when things go wrong during pregnancy.Read moreRead less
FETAL ORIGIN OF ADULT DISEASE? A POPULATION-BASED STUDY OF THE OFFSPRING OF WOMEN WITH SEVERE MENTAL DISORDERS
Funder
National Health and Medical Research Council
Funding Amount
$442,875.00
Summary
Fetal origin of adult disease is a currently influential paradigm in epidemiological research into common diseases (ischaemic heart disease, hypertension, diabetes) and behaviour problems (suicide, criminal offending). It postulates an early pathophysiological programming of outcomes that become manifest in adult life. In the proposed research we aim to examine key aspects of this model by conducting a population-based study on the developmental outcomes, antecedent and concomitant risk factors, ....Fetal origin of adult disease is a currently influential paradigm in epidemiological research into common diseases (ischaemic heart disease, hypertension, diabetes) and behaviour problems (suicide, criminal offending). It postulates an early pathophysiological programming of outcomes that become manifest in adult life. In the proposed research we aim to examine key aspects of this model by conducting a population-based study on the developmental outcomes, antecedent and concomitant risk factors, and a spectrum of neuropsychiatric morbidity in all children (N-5150) born in Western Australia in 1980-2001 to women diagnosed with schizophrenia, bipolar affective disorder or unipolar depression, as compared to children (N-504,553) born to women without a diagnosed psychiatric illness. The study will be based on record linkage, utilising the unique resource of multiple, comprehensive population databases in Western Australia. Specifically, this research will identify the range of developmental outcomes and morbidity in four consecutive birth cohorts (1980-84; 1985-89; 1990-94; and 1995-2001) of children at high genetic and environmental risk and examine their relationship to specific risk factors, including familial genetic load, obstetric complications, severity of maternal illness, and psychosocial adversity. The study will be the first of its kind and its findings will inform aetiological research into the major mental disorders, as well as clinical and public health practice. It will provide novel data on fundamental issues, such as the interaction between genetic risk and environmental factors in the causation of schizophrenia, as well as on the extent to which the risk of developing severe mental illness is immutably embedded in its fetal origin, or is modifiable by subsequent mitigating factors and appropriate intervention.Read moreRead less
Children Of Parents With Mental Illness: A Population-based Study
Funder
National Health and Medical Research Council
Funding Amount
$774,715.00
Summary
Schizophrenia, bipolar disorder and major depression account for about 16% of the global burden of disease, according to estimates by the World Health Organization and the World Bank. These disorders tend to run a chronic or recurrent course, with devastating impact on sufferers and their families. We know today that part of their causes are genetic and may be transmitted to the next generation. However, another part of the causation is likely to be environmental, involving maternal pregnancy co ....Schizophrenia, bipolar disorder and major depression account for about 16% of the global burden of disease, according to estimates by the World Health Organization and the World Bank. These disorders tend to run a chronic or recurrent course, with devastating impact on sufferers and their families. We know today that part of their causes are genetic and may be transmitted to the next generation. However, another part of the causation is likely to be environmental, involving maternal pregnancy complications, as well as psychosocial adversity and stressful events impacting children who happen to carry a genetic susceptibility to such disorders. To disentangle and understand better such effects, our research is focusing on families where genetic risk to the offspring is present, due to a mother suffering from one of these disorders. By linking data available on population databases in WA, we aim to follow up the childhood development and young adult health outcomes of all children born to women with schizophrenia, bipolar disorder or depression. Few studies of this kind have been done worldwide, and we expect that the WA study will answer many unresolved questions, leading to preventative and treatment interventions that would reduce adverse outcomes and improve the quality of life of families at risk.Read moreRead less
Impact Of Chronic Intrauterine Inflammation On Neurodevelopmental & Physiological Responses To Fetal Hypoxia.
Funder
National Health and Medical Research Council
Funding Amount
$280,750.00
Summary
Careful examination of records from hundreds of pregnancies has indicated that low-grade infection or inflammation within the uterus during pregnancy is associated with an increase in the likelihood that the newborn baby will suffer from cerebral palsy. This strong association suggests that inflammation during pregnancy can cause damage to the developing baby's brain. Similar studies have also identified an association betwen events that result in a lack of oxygen supply to the developing brain ....Careful examination of records from hundreds of pregnancies has indicated that low-grade infection or inflammation within the uterus during pregnancy is associated with an increase in the likelihood that the newborn baby will suffer from cerebral palsy. This strong association suggests that inflammation during pregnancy can cause damage to the developing baby's brain. Similar studies have also identified an association betwen events that result in a lack of oxygen supply to the developing brain and cerebral palsy. However the studies that have identified these associations are incapable of determining the mechanisms by which these factors affect brain development. Even though inflammation during pregnancy is common, and is often associated with diseases after birth, experimental studies of the effects of this type of inflammation on the wellbeing of the unborn baby have not been performed. Our research group has developed a unique experimental model, using sheep, which is particularly suitable for determining how inflammation and a lack of oxygen may affect the unborn baby and cause brain damage. By continuously giving a sterile bacterial cell wall preparation (endotoxin) into the amniotic fluid of pregnant sheep we can cause prolonged inflammation with characteristics that are similar to those that accompany inflammation during human pregnancy but different to other models of inflammation within the uterus. We intend to use our model to determine how prolonged inflammation and a lack of oxygen affect the well-being of the developing lamb before birth and how these factors affect brain development. Our proposed study will provide valuable information about how inflammation and a lack of oxygen interact to affect brain development. We expect that when inflammation is present the fetus becomes more vulnerable to the effects of a lack of oxygen, resulting in more severe brain damage occuring than when either factor is experienced alone.Read moreRead less
Neonatal Vitamin D Status And Risk Of Schizophrenia: A Study Using Danish Dried Bloods Spots
Funder
National Health and Medical Research Council
Funding Amount
$164,980.00
Summary
There is increasing evidence that low levels of vitamin D (i.e. the 'sunshine hormone') during early development can alter brain development. In particular, it has been proposed that low vitamin D during development (e.g. prenatal and in early life), increases the risk of developing schizophrenia during adulthood. A previous study based on stored third trimester blood samples from US women suggested that very low levels of maternal vitamin D may be associated with an increased risk of schizophre ....There is increasing evidence that low levels of vitamin D (i.e. the 'sunshine hormone') during early development can alter brain development. In particular, it has been proposed that low vitamin D during development (e.g. prenatal and in early life), increases the risk of developing schizophrenia during adulthood. A previous study based on stored third trimester blood samples from US women suggested that very low levels of maternal vitamin D may be associated with an increased risk of schizophrenia in the offspring. We have the opportunity to explore this hypothesis using a large, well-described Danish 'bio-bank'. Since 1981, blood samples from newborn babies have been kept by a central agency in Denmark. In collaboration with senior Danish medical researchers, 900 blood samples of babies who have subsequently developed schizophrenia and 1800 from matched healthy individuals have been identified. We will measure vitamin D levels in these blood samples. We predict that babies with low levels of vitamin D will have an increased risk of developing schizophrenia. If low prenatal vitamin D does increase the risk of schizophrenia, this finding will have important implications from a public health perspective. Just as the number of infants affected by spina bifida has been reduced by adding folate supplements to foods, optimizing maternal vitamin D levels may lead to a reduction in the incidence of schizophrenia.Read moreRead less
Prenatal Alcohol Exposure: A Molecular Mechanism For Memory Deficits Involving The Zinc-binding Protein, Metallothionein
Funder
National Health and Medical Research Council
Funding Amount
$277,645.00
Summary
Damage to the developing brain is the major social and economic consequence of prenatal alcohol exposure but it is unclear the mechanism by which this occurs. This study will assess whether the maternal zinc-binding protein, metallothionein, causes: 1) alcohol-related cognitive deficits, 2) changes in the expression of alcohol-sensitive cognitive genes. We will further assess whether dietary zinc supplementation throughout pregnancy can prevent alcohol-related anomalies in neurodevelopment.