Hospital Universitario Marques de Valdecilla, Department of Psychiatry, Planta 2a, Edificio 2 de Noviembre. Avda. Valdecilla s/n, 39008, Santander, Spain.
Curr Pharm Des. 2012;18(32):5024-35. doi: 10.2174/138161212802884609.
Cannabis use may be considered as an additional risk factor in a diathesis-stress model of schizophrenia where the risk of developing the illness would be higher in genetic vulnerable people. In this regard, much of the research on cannabis and psychosis is currently focusing on gene-environment interactions. The present review will focus on the interaction between genes and cannabis exposure in the development of psychotic symptoms and schizophrenia and the biological mechanisms of cannabis. Cannabis use has been shown to act together with other environmental factors such as childhood trauma or urbanicity producing synergistic dopamine sensitization effects. Studies on gene-environment interaction have mainly included genetic variants involved in the regulation of the dopaminergic system. The most promising genetic variants in this field are COMT, CNR1, BDNF, AKT1 and NRG1. Additionally, the interaction with other environmental factors and possible gene-gene interactions are considered in the etiological model.
大麻使用可能被视为精神分裂症素质-应激模型中的一个附加风险因素，在遗传易感性人群中，患病的风险更高。在这方面，目前关于大麻和精神病的大部分研究都集中在基因-环境相互作用上。本综述将重点关注基因和大麻暴露在发展为精神病症状和精神分裂症中的相互作用，以及大麻的生物学机制。大麻使用已被证明与其他环境因素（如儿童期创伤或城市化）一起作用，产生协同的多巴胺敏感化效应。关于基因-环境相互作用的研究主要包括参与多巴胺能系统调节的遗传变异。在该领域最有前途的遗传变异是 COMT、CNR1、BDNF、AKT1 和 NRG1。此外，还考虑了与其他环境因素的相互作用以及可能的基因-基因相互作用在病因模型中。
