This is the second series for the Mapping the Pathophysiology of Schizophrenia: Interactions Between Multiple Cellular Pathways Research Topic. Schizophrenia is a complex disorder involving dysregulation of multiple CNS regions and processes in its pathophysiology. Whilst it has been long argued that dopaminergic, glutamatergic, GABAergic and cholinergic neurotransmitter systems are affected in schizophrenia, it is now clear that changes in gene expression in the CNS from patients with schizophrenia will have effects outside of these systems. In addition, it is also becoming clear that external stimuli such as stress and reactive processes such as inflammation, possibly during brain development and later in life, play major roles in the development and exacerbation of symptoms in schizophrenia. These complex cellular pathological processes are now recognised as being brought about because of interactions between disruptions in genetic and epigenetic mechanisms. This hypothesis is consistent with the pathology of schizophrenia being due to the inheritance of a genetic predisposition but with the onset frank symptomatology being triggered by environmental factors. Hence, this special issue will focus on the advancements made within the 10 years since the first Issue in this series on the pathophysiology of schizophrenia was published.
This is the second series for the Mapping the Pathophysiology of Schizophrenia: Interactions Between Multiple Cellular Pathways Research Topic. Schizophrenia is a complex disorder involving dysregulation of multiple CNS regions and processes in its pathophysiology. Whilst it has been long argued that dopaminergic, glutamatergic, GABAergic and cholinergic neurotransmitter systems are affected in schizophrenia, it is now clear that changes in gene expression in the CNS from patients with schizophrenia will have effects outside of these systems. In addition, it is also becoming clear that external stimuli such as stress and reactive processes such as inflammation, possibly during brain development and later in life, play major roles in the development and exacerbation of symptoms in schizophrenia. These complex cellular pathological processes are now recognised as being brought about because of interactions between disruptions in genetic and epigenetic mechanisms. This hypothesis is consistent with the pathology of schizophrenia being due to the inheritance of a genetic predisposition but with the onset frank symptomatology being triggered by environmental factors. Hence, this special issue will focus on the advancements made within the 10 years since the first Issue in this series on the pathophysiology of schizophrenia was published.
