Genetic Risk for Schizophrenia is Connected to Reduced IQ
Reports new study in Biological PsychiatryPhiladelphia, PA, May 16, 2013
The relationship between the heritable risk for schizophrenia and low intelligence (IQ) has not been clear. Schizophrenia is commonly associated with cognitive impairments that may cause functional disability. There are clues that reduced IQ may be linked to the risk for developing schizophrenia. For example, reduced cognitive ability may precede the onset of schizophrenia symptoms. Also, these deficits may be present in healthy relatives of people diagnosed with schizophrenia.
In a remarkable new study published in Biological Psychiatry, Dr. Andrew McIntosh and his colleagues at the University of Edinburgh provide new evidence that the genetic risk for schizophrenia is associated with lower IQ among people who do not develop this disorder.
The authors analyzed data from 937 individuals in Scotland who first completed IQ testing in 1947, at age 11. Around age 70, they were retested and their DNA was analyzed to estimate their genetic risk for schizophrenia.
The researchers found that individuals with a higher genetic risk for schizophrenia had a lower IQ at age 70 but not at age 11. Having more schizophrenia risk-related gene variants was also associated with a greater decline in lifelong cognitive ability.
“If nature has loaded a person’s genes towards schizophrenia, then there is a slight but detectable worsening in cognitive function between childhood and old age. With further research into how these genes affect the brain, it could become possible to understand how genes linked to schizophrenia affect people’s cognitive function,” said McIntosh.
These findings suggest that common genetic variants may underlie both cognitive aging and risk of schizophrenia.
“While this study does not show that these common gene variants produce schizophrenia per se, it elegantly suggests that these variants may contribute to declines in intelligence, a clinical feature associated with schizophrenia,” commented Dr. John Krystal, Editor of Biological Psychiatry. “However, we have yet to understand the development of cognitive impairments that produce disability in young adulthood, the period when schizophrenia develops for many affected people.”
Clearly, more research is necessary, but this new study adds to the growing and substantial effort to understand how the gene variants that contribute to the development of schizophrenia give rise to the cognitive disability commonly associated with it.
The article is “Polygenic Risk for Schizophrenia Is Associated with Cognitive Change Between Childhood and Old Age” by Andrew M. McIntosh, Alan Gow, Michelle Luciano, Gail Davies, David C. Liewald, Sarah E. Harris, Janie Corley, Jeremy Hall, John M. Starr, David J. Porteous, Albert Tenesa, Peter M. Visscher, and Ian J. Deary (doi: 10.1016/j.biopsych.2013.01.011). The article appears in Biological Psychiatry, Volume 73, Issue 10 (May 15, 2013), published by Elsevier.
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Notes for Editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or Biol.Psych@utsouthwestern.edu. Journalists wishing to interview the authors may contact Andrew M. McIntosh at +44 (131) 537 6274 or email@example.com.
The authors’ affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
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