Nature and Nurture
Schizophrenia researchers search for roots of a devastating disorder
By Eva Emerson
When schizophrenia strikes, the brain disorder can leave its victims
struggling with reality, haunted by delusions and auditory
hallucinations and isolated in a world they perceive to have gone mad.
Early theories linked the disease to environmental stresses, such as
growing up in a dysfunctional family. Then, researchers focused their
studies on the brain chemical dopamine, genetics and the brain’s
frontal lobe.
Schizophrenia, says USC College Psychologist Sarnoff Mednick, is a
disease with no simple cause or cure. Today, scientists recognize that
schizophrenia is caused by genetic, biological and environmental
factors. The chronic brain disease affects 1 percent of the U.S.
population, and often does not show itself until late adolescence or
early adulthood.
Mednick was the first to link schizophrenia risk to episodes of
prenatal stress—including exposure to extremely stressful events, like
a massive earthquake.
In 1988, Mednick, director of the Social Science Research Institute at
the College, published a landmark study showing a higher-than-normal
rate of schizophrenia among children whose mothers contracted influenza
in the second trimester of pregnancy.
Mednick, who was awarded the Lieber Prize in Schizophrenia Research,
has since linked prenatal exposures to viruses, intense stress and
radiation to increased rates of a number of psychiatric disorders.
William McClure, professor of biological sciences, uses cellular and
molecular techniques to figure out how prenatal stressors might alter
normal brain development, leading to brain deficits similar to those
associated with schizophrenia.
Recently, McClure’s team found a possible explanation of why
schizophrenia tends to strike people in their late teens and early 20s.
When McClure’s team removed the hormone-producing gonads from rats that
normally develop schizophrenia-like symptoms when they hit “puberty,”
the rats showed no sign of symptoms. The finding leads the team to
believe that sex hormones may play a role in triggering the disease, at
least in animals.
Using psychophysiological approaches, Michael Dawson, professor of
psychology, focuses on finding ways to predict the course of
schizophrenia in patients, in terms of future severity and ability to
function, as well as identifying which patients may be most vulnerable
to relapses. In another project, he wants to see if attention deficits
could be used as a marker of schizophrenia risk.
Psychologist Adrian Raine approaches schizophrenia from another tack,
using brain-imaging techniques to study the brain structure and
function of schizophrenics and people with a “watered-down version of
schizophrenia” called schizotypal personality disorder. His studies
have led him to theorize that damage to the prefrontal cortex, a higher
brain area that inhibits inappropriate behavior and links to the
emotional system, may lead to one or both of the disorders.
Raine and Mednick have also shown the important role the environment
can play in modifying risk: In a long-term study, his team “showed that
enriching the environments of 3-year-olds, by increasing exercise and
cognitive stimulation and improving nutrition for two years, led to a
significant reduction in the incidence of schizotypal personality 20
years later,” says Raine.
“We can treat schizophrenia, but we can’t prevent it. This study gives us, for the first time, a handle on prevention ideas.”
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