It’s not news that stress and depression are linked. It is news, however, that the gene neuritin plays a part in the toxic stress-depression relationship.
All of the clinical antidepressants that are currently on the market work through one specific mechanism: they increase the levels of certain neurotransmitters in your brain.
But it doesn’t help in all people. Only about 1/3 of patients get relief of their symptoms from the first drug they try, and only about 2/3 of patients will be successfully treated even after trying multiple drugs. Of those, many people only get mild relief from their symptoms.
We’re still not exactly sure what causes depression, though, or how antidepressants work. The researchers of this new study decided to see if neuritin plays a role in the process, so they stressed some hapless rats with lights, loud music, uncomfortable temperatures and wet bedding. Compared to a group of control rats, the stressed animals showed decreased neuritin.
In a second experiment, they loaded some rats up with increased neuritin and then stressed them out. Those that were allotted more neuritin expression didn’t exhibit the same depressive behaviors as their stressed but neuritin-lacking counterparts.
While this doesn’t mean that, say, decreased neuritin causes depression (we don’t have any proof of that in humans), it does mean that increasing neuritin by some mechanism might be able to boost antidepressant efficacy, or possibly even make a new antidepressant, though many, many more studies would be needed before that happens.
But neuritin represents an interesting new player in the game of stress and depression, and potentially an interesting new target for studies in humans and animals, and eventually, maybe for new and better antidepressants.
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