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Our perceptions of schizophrenia are often limited to its symptoms that we have observed or heard of: hallucinations, delusions, hearing voices just to name a few. However, the science concerned with how schizophrenia comes about is still in its primitive stages. Psychedelic medicine has been banned since the 1970s in many countries, but has since be reintroduced as new methods to cope with depression, anxiety and nicotine addiction. Now, these psychedelic medicines are also known as psychotomimetics, otherwise known as “mimics of psychosis”. Scientists are hoping that medicinally inducing short and temporary bouts of psychosis in healthy brains will bring them closer to understanding the inner workings of schizophrenia and other mental illnesses on a neural level.
Franz Vollenweider of the University of Zurich and his colleagues hypothesise that schizophrenia is not one, but a group of psychoses that may have different causes. Through the strategy of using psychomimetics to induce bouts of psychosis, they hope to understand the neurological bases of specific symptoms of schizophrenia, so that they will then be able to adjust the medicines prescribed to a person according to what symptoms he or she exhibits.
When some healthy test subjects were given a drug that targets certain effects of the psychoactive ingredient psilocybin in “magic” mushrooms to consume before eating the mushrooms themselves, the visual hallucinations and other typical effects of magic mushrooms were prevented. This existing drug is originally used by patients with anxiety.
There is an urgent need for new treatments for schizophrenia: existing drugs do not treat the less favourable symptoms, such as social isolation, negative thinking and apathy, or even the cognitive impairments that 3 out of 4 afflicted patients face.
It is known that common psychedelics such as LSD and mescaline affect the brain’s serotonin, a neurotransmitter related to mood. Brain scans have found that the neural circuitry for introspection and external attention get tangled up in each other in brains of schizophrenic patients. Similar brain scan results have been reported for healthy people who take these psychedelics. Scientists thus hope that if they can isolate a drug which targets and prevents these boundaries from blurring and bleeding into each other, they will then be able to decode the biological underpinnings of these psychoses.
In one study, 36 people tested one of two antipsychedelic drugs each, either buspirone, a drug usually prescribed for anxiety, or ergotamine, a drug that treats migraines. The scientists were trying to use these drugs as a means of preventing the effects that psychedelics have on serotonin and the resulting hallucinations that people experience. It was found that buspirone was effective in preventing some of the psychotic effects of psilocybin; it has been hypothesised that this is because buspirone binds to serotonin 1A receptors, which then bind to and counteract the serotonin 2A (psilocybin) receptors. Thus, buspirone will suppress the symptoms that are triggered by psilocybin, such as visual hallucinations and imaginative thinking. However, buspirone had no effect on other effects of psilocybin, such as decreased alertness and the fear of going insane that some report.
People with early schizophrenia and Parkinson’s Disease do experience some of the psychotic effects that buspirone can prevent. Pimavanserin, the first approved drug for treating psychotic symptoms in Parkinson’s disease, blocks the serotonin receptor entirely. Another possibility is a blood pressure drug, ketanserin, which blocks the serotonin 2A receptor and suppresses practically all the effects of psilocybin, but has not yet been tested for schizophrenia. It is thus clear that while there is no miracle drug that can cure schizophrenia, there may already be many options available on the market that could curb some of its psychotic symptoms.
Category(s):Schizophrenia
Source material from Scientific American
