Schizophrenia is a mental disorder characterized by a breakdown of thought processes and by poor emotional responsiveness.

People with schizophrenia have such difficulty in sorting out the real from the unreal and in responding to the everyday events of life that they often become immobilized. Sometimes schizophrenia develops slowly as a gradual process of increasing siclusiveness and inappropriate behavior. Sometimes the onset is sudden marked by intense confusion and emotional turmoil. Such acute cases are usually precipitated by a period of stress in individuals whose lives have tended toward isolation, preoccupation with self, and feelings of insecurity. Schizophrenia occurs in all cultures, even those that are remote from the stresses of industrialized civilization. The disorder affects about one percent of the population and occurs equally in men and women. In men, symptoms usually start in the late teens and early 20s. They include hallucinations, or seeing things, and delusions such as hearing voices. For women, they start in the mid-20s to early 30s. Other symptoms include :

Unusual thoughts or perceptions Disorders of movement Difficulty speaking and expressing emotion Problems with attention, memory and organization Understanding the cause of schizophrenia has become more complex. We know

that schizophrenia is caused by genetics factor. However, most people with schizophrenia dont have affected relative. Study about gen and genome recently found that individual genes increase the risk of schizophrenia less than 2 timesfrom the average population rate 1 in 100, and 1,5 in 100. Complications pre-natal and peri-natal, and also environmental exposures increase the risk of schizophrenia from 1 in 100 to 24 in 100. Schizophrenia is likely a result of interaction between genetics factor and environmental exposures, and recent studies attempted to show the interaction. Mki and colleagues studied the interaction between genetics risk (having a parent with schizophrenia) and environmental riskmaternal depression during pregnancy. They found out that maternal depression increases the risk of schizophrenia significantly in offspring, if one of the parent has psychotic disorder. If a child has a parent with psychotic disorder, the risk of schizophrenia increases 2,6 times. The maternal depression itself doesnt increase the risk of schizophrenia. However, if the environmental factorthe maternal depression during pregnancy, and the genetics factor appear simultaneously, the risk of schizophrenia increases 9 times. The

interaction of genetics risk with environmental exposure increase the risk of schizophrenia more than each factor do. This report is the newest from several recent studies describing gene enviroment related to risk for schizophrenia. Including interactions between genetic liability, prenatal exposure to infection, urban birth, and using drugs and a catechol-Omethyltransferase polymorphism. Maki and his friends argue that their result is an indicator of a gene environment interaction between genetic liability and prenatal exposure to depression and stress. There is many fact both in clinical and preclinical studies propose that stress have many effects on brain development that could increase risk for schizophrenia. The authors recognize that it would be one of additive genetic effects that could give a risk depression and probably possible make a risk for schizophrenia. There is increasing general fact about so many genetic risk for schizophrenia. Currently, it is thought that genetic risk for schizophrenia appear in two basic methods. First is polygenic interaction of multiple common variants of probably thousands of genes, each with very small individual effects. Second is the rare but very influence such as deletion or duplication copy of gene. For the enviromental causes schizophrenia most studies have focused on pre- and perinatal environmental risk factors. Three of gene enviromental studies related to schizophrenia focused to infection, depression or stress, and urban birth. What causes schizophrenia? In most cases, schizophrenia is the end result of a complex interaction between thousands of genes and environmental risks. Daniel Weinberger, in his classic paper on brain development and schizophrenia expressed the possibility that schizophrenia was "not the result of discrete events or disease processes at all, but one of the genetic disorders. Schizophrenia is considered a neurodevelopmental disorder subtle brain connectivity, how functional circuits in our brains . Schizophrenia may in fact be the end of the distribution of how the 20 billion neurons and trillions of synaptic connections in our brains produced, removed, and maintained. Presence of disorder in which there is an imbalance in neurotransmitter production of the neurotransmitter dopamine, when the excessive dopamine levels or less, the patient may experience positive symptoms or negative symptoms. Though there is no common cause of schizophrenia now many researchers and doctors believe it results from a combination of the vulnerability of the brain and the environment. What will you do? To treat schizophrenia or to prevent it? The studies give us information about schizophrenia. one strategy, the focus of many current studies, is better understand the roles that risk genes play in brain development.

a parallel approach is the study of how environmental risk factors impact the developing brain. these environmental risk factors can became the best chance at prevention but not for genetic risk factors. clearly more studies of gene-environment interaction, in both clinical samples and in preclinical models are critical. Schizophrenia is likely the result of an abnormal developmental trajectory of synapse and circuit formation that ultimately leads to a miswired brain and clinical symptoms. This abnormal developmental trajectory is contributed to by the interaction of thousands of risk genes and multiple environmental risk factors. Perhaps the best hope to understand and prevent schizophrenia is to focus not so much on the genes or risk factors but rather on the developmental trajectory itself, the final common pathway(s) to schizophrenia. We must understand the periods of human brain development that are important for synapse and circuit development. When do abnormalities in brain wiring actually occur in children at risk for schizophrenia? How do the known environmental and genetic risk factors alter normal developmental trajectories? What are the key transition periods in human brain development? Can we modify developmental trajectories during periods of enhanced plasticity? These and other issues critical to understanding schizophrenia and other psychiatric disorders are discussed in a recent report from the National Institutes of Mental Health: Transformative Neurodevelopmental Research in Mental Illness (11). This approach signifies a bit of a paradigm shift, especially for adult psychiatrists, as it requires a new concentration of efforts on childhood brain development. Only by focusing our research on understanding human developmental trajectories can we develop interventions that recognize and modify, either with pharmacologic or cognitive/behavioral approaches, abnormal developmental trajectories that lead to schizophrenia.