Mapping the pathophysiology of schizophrenia: interactions between multiple cellular pathways

Research on schizophrenia has revealed a variety of risk factors, treatments, and biomarkers that can help elucidate the underlying pathophysiology of the disorder. Studies have identified potential treatments that may improve cognitive deficits, post-mortem brain investigations that can provide insight into the major neurotransmitter systems involved, and the role of BDNF depletion and methamphetamine on sensorimotor gating. Additionally, research has suggested that purine and neurotransmitter metabolism, the development of the prefrontal cortex, and the cholinergic system may be involved in the pathophysiology of schizophrenia. Finally, evidence has been found for complex interactions between cannabis and the schizophrenia candidate gene neuregulin 1 (Nrg1), as well as the involvement of ErbB receptor tyrosine kinases in neurological and psychiatric diseases.

The following highlights can be found in the research:

• D4 receptor-specific antagonists may be able to improve cognitive deficits
• Post-mortem brain investigations can provide insight into major neurotransmitter systems
• BDNF depletion and methamphetamine have different effects on male and female mice
• Purine and neurotransmitter metabolism may be involved in the pathophysiology of schizophrenia
• The development of the prefrontal cortex may be concomitant with cellular and cognitive changes
• Polysialyltransferase (ST8SIA2/ST8SiaII/STX/Siat8B) and its enzymatic product, polySia, may be involved in schizophrenia
• The cholinergic system may interact with other neurotransmitters and inflammation-related factors
• N-methyl-D-aspartate receptor (NMDAR) hypofunction may contribute to the progression and development of symptoms
• Complex interactions between cannabis and the schizophrenia candidate gene neuregulin 1 (Nrg1) have been identified
• ErbB receptor tyrosine kinases may be involved in neurological and psychiatric diseases