Problems in the endocannabinoid system in schizophrenia may result in enhanced sensitivity to psychoactive drugs, and the positive effects of second-generation antipsychotics for drug abuse in schizophrenia may include an alteration of the endocannabinoid system. While people believe that cannabis can cause schizophrenia, studies are showing that a particular chemical compound may be able to treat it.
In this study, 29 patients with schizophrenia and substance use disorders (SUD) were treated with quetiapine (synthetic cannabinoid) for 12 weeks. Endocannabinoid system levels were recorded in patients (weeks 0, 6 and 12) and also 17 healthy volunteers. Cannabinoid levels increased during the study and this helped alleviate some of the schizophrenia symptoms, but only during the treatment.
Improvements in drug abuse were most likely not controlled by the changing effects of quetiapine on the endocannabinoid system. The cannabinoid chemical, anandamide, is a potential target for medications aimed at alleviating some of the stresses of SUD in schizophrenia.
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Schizophrenia is thought to have a part in the destruction in dopamine, glutamate and acetylcholine levels in the brain. These types of neurotransmitters stimulate anandamide levels in rodents. The fact that baseline anandamide levels assumed drug abuse outcomes is of definite interest for future biological studies on schizophrenia.
This result may point at the problems in the endocannabinoid system in schizophrenia may contribute to their enhanced sensitivity to cannabis and alcohol. Also, the predictive value of anandamide makes it a potential go-to place for new pharmacological methods that have a goal of relieving drug abuse in people with or without schizophrenia. In rodents, rimonabant (synthetic cannabinoid) has been shown to reduce alcohol preference, heroin self-administration, and cocaine reinstatement.