Even as my
New York Times Magazine article about deep brain stimulation for depression went to press, a new study came out throwing more light on the "network model" of depression discussed in the article.
In the article I wrote about (among other things) how some interesting work by Andreas Meyer-Lindenberg has begun the work of linking genetic and neurochemical models of depression to the "network" model that’s emerged over the last 5 to 10 years. As the article explains, the neurochemical model, which emphasizes levels of neurotransmitters such as serotonin (the focus of drugs like Prozac), has of necessity focused on brainwide effects so far, while the network or "systems" model focuses on the pathways between particular brain areas.
Meyer-Lindenberg is among those working to merge the two views, and the Times DBS story mentions a paper he did that found that genetic differences affecting the availability of serotonin, the mood-critical neurotransmitter affected by antidepressants such as Prozac, had particular effects in Area 25 — the brain area targeted by the experimental implants described in my Times Magazine story.
Now Meyer-Lindenberg has come out with another paper finding a similar dynamic. In this case, he found that a particular form of the gene — the “L” form — affecting levels of monoamine oxidase (MAO-A) made some people react to stress more violently and aggressively than others. One key difference was that people with the L version often showed more activity in their amygdalas, a mid-brain area associated with fear. (For more on the amygdala, see my story on Joseph LeDoux.) Fear and anxiety, of course, are crucial in depression; they seem to form much of the “active anguish” that William James speaks of, and that makes depression so hard to live with. This MAO-A L variant, though, seemed to turn that fear and anxiety outward.