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Classic psychedelics, like LSD and psilocybin from psychedelic mushrooms, activate 5-HT2A "psychedelic" serotonin receptors in the brain, which cause psychedelic effects (like hallucinations) and therapeutic effects (e.g. reduced depressive symptoms).
Activation of 5-HT2A receptors stimulates neurons to grow new branches and form new connections with other neurons in a process called 'neuroplasticity'. This rewiring of neural connections can occur within days and the benefits can last for months; it is also thought to underpin the anti-depressant effects that are being observed in clinical trials with psychedelics.
However, activation of 5-HT2A receptors also causes intense perception-distorting effects, which require psychedelic therapies to be administered under clinical supervision (i.e. making treatment prohibitively expensive) and deem them inappropriate for people who are sensitive to hallucinations (e.g. individuals at risk of psychosis). Thus, the therapeutic use of psychedelics is limited by their hallucinatory effects.
Tweaking the chemical structure of existing psychedelic molecules is predicted to yield compounds that activate the 5-HT2A receptor, increase neuroplasticity and treat depression without causing hallucinations. Non-hallucinogenic 5-HT2A anti-depressants will not replace existing classic psychedelic-assisted psychotherapies but will complement them in a suite of personalized treatment options.
In the hope to develop anti-depressants that can benefit broader populations, biotech companies like Psylo are using innovative strategies to develop novel 5-HT2A antidepressants that don't induce strong hallucinatory effects. These promising compounds are progressing through early R&D and are expected to enter clinical trials in the coming years.
For more information, see Taking the tripping out of psychedelic medicine
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