Every in such a manner often there comes a truly “headdesk” import in science. A moment where you be there, stunned by a new verdict, and thinking, blankly…”OK, at present what?” For psychiatry and behavioral pharmacology, united of those moments came a scarcely any weeks ago with the findings of a meta-calculus published in the British Medical Journal (Eyding et al., 2010). The meta-analytics showed that an antidepressant, reboxetine (marketed through Pfizer in Europe, but not in the U.S., when exposed to the names Edronax, Norebox, Prolift, Solvex, Davedax or Vestra) doesn’t act. Not only does it not moil, it really doesn’t work, and it turns to the end that Pfizer hadn’t published given conditions on the putative antidepressant from 74% of their patients.
It turns on the ~side that publication bias was rampant. Pfizer and Lundbeck, the couple companies running the studies, didn’t make known a lot of their data, especially the data showing no effect and unfortunate edge effects. A bit nefarious, that.
this is a sharp moment for scientists studying depression. Why? Because reboxetine works beautifully in our created being models. It’s practically a poster-infant antidepressant. It produces acute effects in tests in the same state as forced-swim tests and horse-~-suspension tests (which use changes in struggle similar to a measure of antidepressant efficacy). It produces neurogenesis in the hippocampus, that is thought to be correlated by antidepressant effects. When behavioral pharmacologists are doing comparisons betwixt older antidepressants and newer ones, reboxetine is frequently used as a positive control, a physic known to have an effect in the behavioral touchstone of choice.
But it doesn’t drudge in patients. And patients are what matters. Now, scientists are stuck by a difficult question: What went sin? This is more than just some issue with an antidepressant that didn’t toil, it’s an issue with the tests we are using to study pit. How effective are they, really? Are we in act modeling the right things? Do the lower part-suspension test and forced-swim standard detect antidepressant activity after all? And if they aren’t detecting antidepressant etc., what are they actually doing? What does this low for both the neurochemical theory of lowness and the neurogenesis theory?
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