Emptiness. It is a word that many people with depression are familiar with. It is characterized by a distinct feeling of being lacking – lacking in feeling, lacking in motivation, lacking essential internal components that can make you feel “normal.” Ironically, researchers have found that it is an excess of a certain protein in the brain that may be a major factor in the development of depression in individuals.
The protein in question is called fibroblast growth factor 9, or FGF9 for short. When researching the protein, scientists found that people with major depression had 32% more of this protein in certain parts of their brain.
Testing the theory
Researchers from many organizations and universities, including the University of Michigan Medical School and the Pritzker Neuropsychiatric Disorders Research Consortium, developed their theory on FGF9 after years of studying brain tissue samples. They found that, along with increased levels of FGF9, the section of the brain called the hippocampus was smaller in brain samples of depressed individuals. They theorize that this is the result of FGF9 blocking cell growth and development in the brain.
In order to get a firm grasp on what FGF9 does to the brain, researchers used rats to see how changing the levels of the protein in their brains modified behavior. First, they exposed the rats to increased social stress for a week-long period. They found that FGF9 levels did increase, and the subjects became more socially withdrawn.
Next, the researchers injected FGF9 into the brains of an experimental rat group; the control group was given a placebo. The rats that received the real injection became much more anxious and less motivated to move around. These symptoms only worsened with more injections.
Finally, the researchers created a virus that would interfere with FGF9 production in the brain. They injected it into an experimental group of rats and found that FGF9 levels decreased by 30%. These rats became much less anxious as a result.
If we take a cue from the last experiment mentioned, then we can begin to see what some of the benefits of this research could be. It has already gone a long way in proving that depression is a physical illness, which has been debated in the medical community for many years.
“Fixing depression is not easy, because it’s a disorder at the level of the circuits that connect brain cells, and many regions of the brain are involved,” said Elyse Aurbach, co-author of the paper. “Still, this is the first time FGF9 has been identified as related to depression, and found to be active in a critical area of the brain for the disorder. We and others need to study it further to determine what is going on. It’s very exciting.”
As Aurbach says, there is still much research to be done on FGF9 before any sort of antidepressant can be developed. But when antidepressants can be developed, they would be much safer. Because the new medication would work at inhibiting FGF9 levels, instead of decreasing levels of something else in the brain, the risk of side effects would be greatly reduced. This thought will no doubt spur researchers on and keep them cautiously optimistic.