When studying depression, researchers tend to focus on what is missing from the patients, like maybe (but probably not) serotonin, or brain-derived neurotrophic factor (“brain fertilizer”)—but far fewer investigate what the brain has more of.
This means that a new study published in the Proceedings of the National Academy of Sciences is one of the first to suggest that having too much of an essential molecule might lead to depression, and it offers a strong solution for treatment.
A team from the University of Michigan Medical School and the Pritzker Neuropsychiatric Disorders Research Consortium discovered that the brains of people suffering from depression had high levels of a protein known as FGF9 (fibroblast growth factor 9) while thoroughly examining cadaver brain tissue. The main focus was the hippocampi of the brains—the part that shrinks in depression—which were donated by 36 people with and 56 without major depression.
“We call this approach ‘reverse translation’,” said author Huda Akil, a professor of psychiatry and neuroscience. “We start by careful, broad scale analyses in the human brain to discover new molecular players that might play a role in triggering or maintaining the depression.”
Using this technique, they found that FGF9 exists in amounts 32% higher in the hippocampi of depressed brains than in those without it. Further, several other fibroblast growth factors showed decreased expression, which suggests that the whole system necessary for regulating cell growth and development is altered in depression.
The rats confirm it… and solve it?
But the researchers didn’t just stop here. Intrigued by the results, they decided to do multiple experiments in rats to see if these findings held.
They exposed rats to repeated stress for a week and a half (stress is one of the top causes of depression), and found that the levels of FGF9 rose, thus coinciding with socially withdrawn behavior and changes in weight.
Then, they injected FGF9 or a placebo directly into the ventricles (the fluid-filled cavities between the two halves of the brain) of the rats. The FGF9 rats became more anxious, and began to move much less—changes that continued to show up with repeated injections.
The most exciting study, however, was when they injected a virus into the rat hippocampi. The virus was of two types: One that blocked FGF9 expression, and one that was an inactive control. In the FGF9-blocking virus, the levels of the protein dropped nearly 30% as compared to the inactive-virus, and those mice showed less anxiety to boot.
With all these results, the researchers believe that this provides even more evidence that depression goes far beyond something just in your head, or a chemical imbalance; it is a physical illness.
So is this the cure for depression? Probably not—there’s a lot about it we don’t understand. But the research team is optimistic.
“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 co-author Elyse Aurbach, a neuroscience doctoral student. “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.”
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