New laboratory research on rodents suggests an elevated stress hormone in adolescence may be linked to severe mental illness in adulthood.
Johns Hopkins researchers noted that adolescence is a critical time for brain development. During this stage, a hormone abundance could potentially cause genetic changes which could result in severe mental illness among individuals.
The findings, reported in the journal Science, could have wide-reaching implications in both the prevention and treatment of schizophrenia, severe depression and other mental illnesses.
“We have discovered a mechanism for how environmental factors, such as stress hormones, can affect the brain’s physiology and bring about mental illness,” said study leader Akira Sawa, M.D., Ph.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine.
“We’ve shown in mice that stress in adolescence can affect the expression of a gene that codes for a key neurotransmitter related to mental function and psychiatric illness. While many genes are believed to be involved in the development of mental illness, my gut feeling is environmental factors are critically important to the process.”
“Genetic risk factors in these experiments were necessary, but not sufficient, to cause behaviors associated with mental illness in mice,” Sawa said. “Only the addition of the external stressor — in this case, excess cortisol related to social isolation — was enough to bring about dramatic behavior changes.”
The investigators not only found that the “mentally ill” mice had elevated levels of cortisol, known as the stress hormone because it is secreted at higher levels during the body’s fight-or-flight response, but that these mice had significantly lower levels of the neurotransmitter dopamine in a specific region of the brain involved in higher brain function, such as emotional control and cognition. Changes in dopamine in the brains of patients with schizophrenia, depression and mood disorders have been suggested in clinical studies, but the mechanism for the clinical impact remains elusive.
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