Depression has long been associated with a lack of certain chemicals in the brain. However, new University research suggests depression may involve too much of one specific protein.
Elyse Aurbach, a neuroscience graduate student, and Edny Inui, who earned her PhD at the University, found FGF9 levels were markedly increased in the brains of depressed individuals.
Aurbach and Inui looked at post-mortem brain tissue in people who had had depression and in people who did not, and discovered different levels of a protein called fibroblast growth factor 9. Aurbach said this method had its limitations — it was not possible to determine if high levels of FGF9 caused depression or were an effect of depression.
“The problem with looking at post-mortem human brains is that we could not tell the difference between something that predisposes someone toward getting depression versus a result of a person having had depression for years,” Aurbach said.
To address this limitation, researchers did further experiments with live rats. They observed three key findings. When rats were exposed to social stress, they showed increased levels of FGF9 in the hippocampus, the part of the brain associated with emotion and memory. If injected with FGF9, rats displayed increased anxiety — a common symptom of depression.
The third key finding: After using a virus to interfere with FGF9 production, the rats’ anxiety decreased.
These experiments showed increased FGF9 is not only a result of depression, but can actually cause depression in rats. As a result, Aurbach said this discovery has far-reaching implications.
“This study reinforces the idea that depression is a physical illness of the brain,” she said. “It is not a problem of willpower or of people being able to snap their fingers and adopt a different coping strategy.”
Inui, co-author of the study, said the findings of the paper offer potential for designing novel therapeutics. The results are especially promising because it is safer to design drugs that block the actions of something harmful rather than those that increase the actions of something beneficial.
“It is a lot easier from a drug perspective to knock that expression down than it is to increase the expression of another target,” she said. “That can potentially have many more side effects.”
Central to this study is its connection to the lives of college students, Aurbach said. Faced with the task of succeeding academically while maintaining social and extracurricular commitments, college students experience numerous stressors that can lead to a wide variety of mental health issues.
LSA senior Anna Chen is the president of the University’s chapter of Active Minds at the University of Michigan. This nonprofit organization is dedicated to raising awareness for mental health issues among college students.
Chen said she is very excited for the therapeutic potential of the study. Even so, she recognizes there is no “quick fix” for mental illness.
“The causes of any mental illness are multifaceted,” Chen said. “I hope that the increasing effectiveness of medications doesn’t cause people to devalue the benefit of supplementing psychiatric treatment with behavioral therapy.”
In the future, Aurbach said she aims to better understand how FGF9 is functioning in more areas of the brain and whether FGF9 is working with or against other molecules in the brain to change behavior.
“If we can understand how FGF9 is involved in all areas of the brain, then we can build a much bigger picture of how we can develop a drug to target depression effectively,” she said.