This week, Finnish scientists announced an exciting breakthrough in their studies of depression that might provide a new approach to anti-depressants in the future. They centered their attention on neurogenesis, the production of new nerve cells in the brain, which previous research has shown might play a role in anxiety and depression in the brain's hippocampus: it seems to be impaired in those with certain mood disorders.

They found that a particular kind of protein, Jun N-terminal kinases (or JNK), is responsible for moderating neurogenesis in the hippocampus, and so seems directly responsible for anxious and depressive behavior. When they fiddled with it, they found that inhibiting it produced positive mood responses: the mice with their JNK inhibited had lower anxiety levels and more neurogenesis. And by "more" they mean "much more:" cell proliferation, they reported, "increased by 80% and survival by 200% at 6 weeks" after the JNK treatment. The scientists think that the combination of JNK inhibition and the new bunch of cell growth produces a "powerful neurogenic stimulus" that helps mood disorders.

This is particularly intriguing because JNK is at the forefront of a variety of disease studies. In a 2003 study called, hilariously, "From Junk To Gold," JNK inhibition was mentioned to be possibly helpful for "inflammatory, vascular, neurodegenerative, metabolic and oncological diseases in humans," and now we might be able to add mood disorders to that list. It's a complete departure from the tendency of antidepressants to target neurotransmitters, but what a protein inhibitor pill would look like, and how it would work in humans, remains unknown. Stay tuned.

Wouldn't it be useful if we knew whether a particular kind of antidepressant would work before somebody started a course on it? We might be able to. A particular kind of brain processing pattern detectable in MRIs is, according to new science from the University of Illinois, a sign that normal anti-depressant therapy won't be effective in a patient. The pattern, interestingly enough, pops up when we make an error, and shows communication between parts of the brain associated with mistake detection and information processing.

Thirty-six adult patients with depression and no drug regime were given a series of tests while having an MRI, then given varieties of antidepressants and monitored over months for the usefulness of the treatment. Interestingly, there was a high correlation between those patients who showed the brain pattern in response to error and those who showed little response to traditional drug treatment.

The pattern itself, the scientists suggest, may be demonstrating a powerful tendency to "ruminate" over mistakes or make negative inferences from them. The depression-rumination cycle, the American Psychological Association says, is a key component of serious depressive disorder, in which negative experiences and self-talk are constantly reiterated and revisited in the brain, depleting mood. Traditional antidepressants don't really target rumination behavior, but an overview of the next wave of antidepressants in 2013 noted that ketamine shows promise as a possible treatment for it in depressives. If enough of these therapies develop in tandem, brain scans can help depressives be placed onto drugs that accurately reflect the specific patterns of their mood disorders, and so have better experiences.

The world of options opening up to those who aren't responding to antidepressants doesn't require entirely new drugs, though. At least that's according to a bit of science released in November 2016, in which bipolar people in the depressive phase of their disorder who had previously been unresponsive to antidepressants were helped by an unexpected source: an arthritis drug.

Celecoxib, an anti-inflammatory drug given to arthritis sufferers, was given to a portion of the study group alongside the antidepressant Lexapro, while the other portion was given Lexapro and a placebo. After a few weeks, 45 percent of the placebo group reported a significant lift in their depression and 10 percent indicated it had gone away completely. But that was dwarfed by the experiences of the celecoxib group: 78 percent of them experienced a massive drop in their depressive symptoms, while 63 percent reported its total removal. That's massive.

The scientists behind the test think it has to do with the role of inflammation in neurotransmitter performance. Neurotransmitters are the things targeted by SSRIs like Lexapro, and significant science has already been done linking chronic low-grade inflammation in the body to experiences of depression. The anti-inflammatory effects of celecoxib banished the inflammation, helped neurotransmitter improve their performance, and kicked depression out of the ballpark.

This is cool because it's a therapy that can actually be useful now. Tests for low-grade inflammation do exist, so if your antidepressant isn't working sufficiently and you have a doctor willing to look at the latest science, they might be able to test you for it and experiment with adding arthritis drugs to your dosage. It's a highly experimental therapy that needs to be undertaken carefully (and note that the study only involved bipolar people, not people with major depressive disorder), but it's a very interesting start.