To conduct their study, scientists—led by Myrna Weissman, professor of epidemiology in psychiatry at the Columbia University College of Physicians and Surgeons, and director of the division of epidemiology at the New York State Psychiatric Institute—imaged the brains of 131 individuals, including 12 children, roughly half of whom had a strong family history of depression.
The research showed that not only was the frequency of depressive symptoms significantly greater in the high-risk group than in the low-risk group, but the magnetic resonance imaging scans revealed broad expanses of thinning in the cortex, specifically in the brain’s right hemisphere. The cortex is the outermost portion of the brain and has been linked to the development of depression by previous research. The right hemisphere, in particular, is thought to facilitate the perception of social and emotional stimuli from the surrounding environment.
The paper, “Cortical thinning in persons at increased familial risk for major depression,” published on the Proceedings of the National Academy of Sciences’ Web site on March 27, proposes that the thinning of the cortical tissue in the right hemisphere likely detracts from an individual’s ability to process these stimuli, predisposing that individual toward depression. A similar reduction in thickness in the corresponding portions of the left hemisphere of the brain is required to produce depressive symptoms, the study states.
The paper identifies cortical thinning as a biomarker—a biological indicator of disease—for only the familial form of depression, which constitutes the majority of depression cases seen clinically.
While the reduction in cortical thickness is not the first biological indicator of depression ever found, it is “certainly one of the strongest,” said Bradley Peterson, director of child and adolescent psychiatry at the Columbia University Medical Center and the paper’s first author. The thinning is remarkable for the amount of space it covers, but most significantly, it is present in the offspring of depressed individuals, even if those descendants haven’t experienced symptoms themselves, Peterson said.
“It’s not a consequence of having been depressed, it’s not a consequence of treatment—it is there early in life, and it seems to be something that contributes to cognitive problems and subsequently becoming symptomatic,” he emphasized.
While cortical thinning may be a familial trait, it is not necessarily genetically inherited, Peterson said. “We don’t know what the ultimate source is—whether it’s a genetic cause, or growing up in a depressed environment, or something else. But whatever that cause is, it’s having a hardwiring effect in the brain from early childhood.”
The question of whether this thinning can be considered a marker for depression in general remains largely unanswered, but the study suggests that this may be the case.
Within the low-risk group, there were individuals who had developed depression over the course of their lifetimes despite the fact that they had no strong family history of the illness. When the brains of these individuals were compared to the brains of others in the low-risk group who had never been depressed, right hemisphere thinning was still found.
Still, the implications of this finding on the future of clinical depression treatment remains unknown. “A key direction for research would be to try and develop therapies that will either minimize or reverse the anatomical abnormalities that we’re seeing,” Peterson said. The brain is a highly plastic organ, and it is possible that cognitive training exercises could strengthen the right hemisphere and provide compensation for the defects that the thinning seems to cause, Peterson said.
In addition, the study opens the door to further research on biomarkers for different subtypes of depression, which could allow for more individualized treatments in the future, he concluded.
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