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WHAT CAUSES SCHIZOPHRENIA?

There is no known single cause of schizophrenia. Many diseases, such as heart disease, result from an interplay of genetic, behavioral, and other factors; and this may be the case for schizophrenia as well. Scientists do not yet understand all of the factors necessary to produce schizophrenia, but all the tools of modern biomedical research are being used to search for genes, critical moments in brain development, and other factors that may lead to the illness.

Is Schizophrenia Inherited?

It has long been known that schizophrenia runs in families. People who have a close relative with schizophrenia are more likely to develop the disorder than are people who have no relatives with the illness. For example, a monozygotic (identical) twin of a person with schizophrenia has the highest risk – 40 to 50 percent – of developing the illness. A child whose parent has schizophrenia has about a 10 percent chance. By comparison, the risk of schizophrenia in the general population is about 1 percent.

Scientists are studying genetic factors in schizophrenia. It appears likely that multiple genes are involved in creating a predisposition to develop the disorder. In addition, factors such as prenatal difficulties like intrauterine starvation or viral infections, perinatal complications, and various nonspecific stressors, seem to influence the development of schizophrenia. However, it is not yet understood how the genetic predisposition is transmitted, and it cannot yet be accurately predicted whether a given person will or will not develop the disorder.

Several regions of the human genome are being investigated to identify genes that may confer susceptibility for schizophrenia. The strongest evidence to date leads to chromosomes 13 and 6 but remains unconfirmed. Identification of specific genes involved in the development of schizophrenia will provide important clues into what goes wrong in the brain to produce and sustain the illness and will guide the development of new and better treatments. To learn more about the genetic basis for schizophrenia, the NIMH has established a Schizophrenia Genetics Initiative (see Web site at http://www-grb.nimh.nih.gov/gi.html) that is gathering data from a large number of families of people with the illness.

Is Schizophrenia Associated With A Chemical Defect In The Brain?

Basic knowledge about brain chemistry and its link to schizophrenia is expanding rapidly. Neurotransmitters, substances that allow communication between nerve cells, have long been thought to be involved in the development of schizophrenia. It is likely, although not yet certain, that the disorder is associated with some imbalance of the complex, interrelated chemical systems of the brain, perhaps involving the neurotransmitters dopamine and glutamate. This area of research is promising.

Is Schizophrenia Caused By A Physical Abnormality In The Brain?

There have been dramatic advances in neuroimaging technology that permit scientists to study brain structure and function in living individuals. Many studies of people with schizophrenia have found abnormalities in brain structure (for example, enlargement of the fluid-filled cavities, called the ventricles, in the interior of the brain, and decreased size of certain brain regions) or function (for example, decreased metabolic activity in certain brain regions). It should be emphasized that these abnormalities are quite subtle and are not characteristic of all people with schizophrenia, nor do they occur only in individuals with this illness. Microscopic studies of brain tissue after death have also shown small changes in distribution or number of brain cells in people with schizophrenia. It appears that many (but probably not all) of these changes are present before an individual becomes ill, and schizophrenia may be, in part, a disorder in development of the brain.

Developmental neurobiologists funded by the National Institute of Mental Health (NIMH) have found that schizophrenia may be a developmental disorder resulting when neurons form inappropriate connections during fetal development. These errors may lie dormant until puberty, when changes in the brain that occur normally during this critical stage of maturation interact adversely with the faulty connections. This research has spurred efforts to identify prenatal factors that may have some bearing on the apparent developmental abnormality.

In other studies, investigators using brain-imaging techniques have found evidence of early biochemical changes that may precede the onset of disease symptoms, prompting examination of the neural circuits that are most likely to be involved in producing those symptoms. Meanwhile, scientists working at the molecular level are exploring the genetic basis for abnormalities in brain development and in the neurotransmitter systems regulating brain function.

Next: How Is It Treated?


Resources: Information, support, and advocacy organizations:

NAMI
Colonial Place Three
2107 Wilson Blvd., Suite 300
Arlington, VA 22201-3042
Phone: 1-800-950-NAMI (6264) or (703) 524-7600
Internet: http://www.nami.org

National Mental Health Association (NMHA)
1021 Prince Street
Alexandria, VA 22314-2971
Phone: 1-800-969-6942 or (703) 684-7722
Internet: http://www.nmha.org

National Mental Health Consumers' Self-Help Clearinghouse
1211 Chestnut Street, Suite 1000
Philadelphia, PA 19107
Phone: 1-800-553-4key (4539) or (215) 751-1810
Internet: http://www.mhselfhelp.org/index2.html

National Alliance for Research on Schizophrenia and Depression (NARSAD)
60 Cutter Mill Road, Suite 404
Great Neck, NY 11021
Phone: (516) 829-0091
Internet: http://www.narsad.org

For more information on research into the brain, behavior, and mental disorders contact:

National Institute of Mental Health (NIMH)
Office of Communication and Public Liaison
Information Resources and Inquiries Branch
6001 Executive Boulevard, Rm. 8184, MSC 9663
Bethesda, MD 20892-9663
Phone: 301-443-4513
Fax: 301-443-4279
E-mail: nimhinfo@nih.gov
Fax back system: Mental Health FAX4U at 301-443-5158
Web site address: http://www.nimh.nih.gov

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