Schizophrenia: A Disorder of Neurodevelopment and Accelerated Aging?
Suggests a new study in Biological Psychiatry
Philadelphia, PA, March 6, 2013 – Many lines of evidence indicate that schizophrenia is a disorder of neurodevelopment. For example, genes implicated in the heritable risk for schizophrenia are also implicated in the development of nerve cells and their connections. Numerous findings in brain imaging studies describe the changes in brain structure and function associated with schizophrenia as emerging early in the course of the disorder. Some early brain imaging studies even found little or no evidence of progression of structural deficits.
Yet, a new generation of studies now also describes degenerative processes in schizophrenia that resemble accelerated aging. Schizophrenia is associated with an increased risk of cardiovascular illnesses and persons with schizophrenia have shorter average lifespans. Studies have also found that individuals with schizophrenia have shortened telomeres, a marker of aging. Structural imaging studies describe enhanced reductions in gray and white matter volumes and increased cortical thinning with age associated with schizophrenia. Similar findings have also emerged for individuals diagnosed with major depressive disorder.
This evidence led researchers of a new study in Biological Psychiatry to specifically examine age-related decline in cerebral white matter in schizophrenia and major depressive disorder, using a measure of microstructural integrity called fractional anisotropy. For comparison, they recruited two normal control groups, one for each cohort.
Dr. Peter Kochunov, first author of the study, explained their findings: “This study showed that the brain's white matter, or the wiring of the brain, ages faster in patients with schizophrenia compared with people who do not have a mental illness. In comparison, the white matter in people with major depression ages similarly to people without a mental illness.”
“We are getting a clear picture that a component of the biology of schizophrenia progresses with age. However, I am afraid that we have relatively little understanding of how or why this progression occurs. Thus, it seems that we are at the beginning of exploring a new dimension of the illness that may hold clues to preventing functional decline associated with schizophrenia,” commented Dr. John Krystal, Editor of Biological Psychiatry.
Kochunov agrees, adding that they already have additional work planned. “Our next step is to find the cause of this disease-specific effect on accelerated aging by schizophrenia and determine whether it relates to the cause or the consequence of schizophrenia.”
The article is “Testing the Hypothesis of Accelerated Cerebral White Matter Aging in Schizophrenia and Major Depression” by Peter Kochunov, David C. Glahn, Laura M. Rowland, Rene L. Olvera, Anderson Winkler, Yi-Hong Yang, Hemalatha Sampath, Will T. Carpenter, Ravindranath Duggirala, Joanne Curran, John Blangero, and L. Elliot Hong (doi: 10.1016/j.biopsych.2012.10.002). The article appears in Biological Psychiatry, Volume 73, Issue 5 (March 1, 2013), published by Elsevier.
# # #
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 Peter Kochunov at 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.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 5th out of 129 Psychiatry titles and 16th out of 243 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2011 Impact Factor score for Biological Psychiatry is 8.283.
Elsevier is a global information analytics business that helps scientists and clinicians to find new answers, reshape human knowledge, and tackle the most urgent human crises. For 140 years, we have partnered with the research world to curate and verify scientific knowledge. Today, we’re committed to bringing that rigor to a new generation of platforms. Elsevier provides digital solutions and tools in the areas of strategic research management, R&D performance, clinical decision support, and professional education; including ScienceDirect, Scopus, SciVal, ClinicalKey and Sherpath. Elsevier publishes over 2,500 digitized journals, including The Lancet and Cell, 39,000 e-book titles and many iconic reference works, including Gray's Anatomy. Elsevier is part of RELX Group, a global provider of information and analytics for professionals and business customers across industries. www.elsevier.com
Editorial Office, Biological Psychiatry+1 214 648 0880