Investigating environmental-genetic interactions in schizophrenia development and etiology.
Research into the pathogenesis of schizophrenia has revealed a number of potential causes, including abnormalities in the GABA system, the adenosine hypothesis, and modulation of histone acetylation. Recent studies have also suggested that activating muscarinic M1 and M4 receptors, and miR-25-3p-mediated signaling pathways, may reduce the severity of schizophrenia symptoms. Cannabidiol (CBD) has potential to prevent schizophrenia development, although it may contribute to pathological changes in the brain. Finally, clozapine may act by normalizing perturbations in the glutamatergic signaling pathway.
This research topic has revealed a number of potential causes of schizophrenia, including:
- Abnormalities in the GABA system
- The adenosine hypothesis
- Modulation of histone acetylation
- Activating muscarinic M1 and M4 receptors
- miR-25-3p-mediated signaling pathways
- Cannabidiol (CBD)
These potential causes are being investigated to determine their contribution to the pathogenesis of schizophrenia, and to develop new treatments for the disorder.