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On December 29, 1987 - 30 years ago - a new antidepressant from the pharmaceutical company Eli Lilly received its approval in the USA. It was called Prozac. The prefix "Pro" suggests something positive, combined with "zac" it works quickly and effectively. The market launch was accompanied by a massive advertising campaign and it had an impact: Prozac became an icon. It graced the front page of magazines, was sung about in pop songs, and Prozac stories became bestsellers and box office hits. Late effects of the boom: Today around twelve percent of Americans swallow antidepressants.
Eli Lilly's marketing strategy was based on a mistake. At that time, psychiatrists saw the cause of depression in a lack of certain messenger substances in the brain: norepinephrine and, above all, serotonin. Eli Lilly advertised that Prozac, with its active ingredient fluoxetine, specifically restores the serotonous balance. Prozac was the first representative of these so-called selective serotonin reuptake inhibitors, or SSRIs for short. There are now a number of drugs with this principle of action.
Today we know, however, that a lowered serotonin level alone does not explain depression. "SSRIs increase the serotonin level within a few hours. If that were the active principle, the mood of the patient should improve very quickly," says Peter Gass, scientist at the Central Institute for Mental Health in Mannheim. However, this is not the case, a clinical effect only occurs after weeks and only in about sixty percent of the patients. So SSRIs only fight depression very indirectly. But how exactly?
"I like to compare that with dominoes - an increased serotonin level influences a number of molecular processes in the brain cells, which are then important for the actual therapeutic effect," says Christoph Turck from the Max Planck Institute for Psychiatry in Munich. Antidepressants, when they are successful, stimulate neural plasticity - that is, the ability of nerve cells to form new connections and thus react flexibly to external factors.
Persistent stress is a common cause of depression. Stress hormones permanently damage neuronal structures in certain areas of the brain. "Such changes then affect the brain circuits - including those that regulate mood," says Turck. In order to cure depression, it is important to counteract these changes in the brain. Scientists are therefore placing their hopes in a drug that stimulates plasticity much more directly: ketamine. The drug has long been used in anesthesia and pain management. In 2006, scientists from the National Institute of Mental Health in the USA showed for the first time in a systematic study that it also works as an antidepressant.
Ketamine leads to the release of glutamate at the synapses - a widespread messenger substance in the brain that plays an important role in the neuronal plasticity of almost all nerve cells. "Ketamine has a lot of potential, it works quickly and effectively - even in depressed patients who do not respond to other antidepressants and are considered treatment-resistant," says Ronald Duman of the Yale University School of Medicine in New Haven, Connecticut (USA). Ketamine has not yet been approved for the treatment of depression due to the lack of clinical studies. It is still used in some private clinics off label offered.
"For many treatment-resistant patients, ketamine is already the way out of depression. But there is still potential for further development," says Gass. Because ketamine has side effects. It can trigger psychotropic effects, has a dissociative effect and is therefore also known as an intoxicating drug. "The task now is to develop new substances that maintain the antidepressant effect of ketamine but minimize the side effects," explains Gass. To do this, you first have to understand very precisely how ketamine works in the brain. "Science has made enormous progress here," says Gass. And yet there is still a long way to go.
Turck is addressing another question of clinical relevance: which drug helps which patients? Together with his team, he is looking for biomarkers that predict whether a patient will respond to an antidepressant. "We pursue a pragmatic approach, which should enable the psychiatrist to help quickly with the right medication in order to reduce the suffering of the patient in a timely manner," said Turck.
30 years ago Eli advertised Lilly to counter depression by raising the serotonin level. Today we know that this is not enough. Scientists are now looking at another mechanism - plasticity. But that doesn't solve all the riddles by a long shot. "We are still a long way from understanding how the brain works and what exactly goes wrong with mental illness," says Turck. The miracle cure, which intervenes in neural processes in such a way that it causes the cause of depression, will not be around for a long time. The treatment of depression is still far from "pro" and "zac".
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