Numerous lines of evidence implicate myelin and oligodendrocyte function as critical processes affecting neuronal connectivity, which is a central abnormality in schizophrenia. Neurodevelopmental models related to dysmyelination have suggested its relation with different schizophrenia-like symptoms. Post-mortem studies in patients with schizophrenia have reported 14–22% reduction in the density and the quantity of oligodendrocytes. Several myelin-related candidate genes have been linked oligodendrocyte and myelin dysfunction with neu- rocircuitry abnormalities in schizophrenia. A number of myelin gene knockout mice models exhibit schizophrenia-like behaviours, and genomic, especially GWAS, studies identified new schizophrenia loci related to oligodendrocyte genetic polymorphisms. It is known that myelin acts as electrical insu- lation for the ensheathed axon, which helps to preserve the amplitude and to increase the conduction velocity of the propagating axon potential. A growing body of evidence points towards the involve- ment of dysmyelination of the prefrontal cortex in the development of the cognitive symptoms of psychosis. Neuroimaging investigations have linked processing speed to brain anatomical connectivity, and have pointed the role of processing speed among the predictors of clinical changes in schizo- phrenia. The dysmyelination-induced delays in patients with psychosis may cause a discrepancy in sensory feedback mechanisms, which results in prediction error. The myelin abnormalities and the resulting conduction delays vary during the course of the multiple sclerosis and this type of cycles are possibly associated with fluctuations in conduction velocity in psychosis. It is worthy of note that the major histocompatibility complex (MHC) is responsible for the genetic overlap in both multiple sclerosis and schizophrenia. Multiple sclerosis manifests sensory and motor symptoms, and schizophrenia disordered cognition and emotion. Having in mind the interdependent relationship of oligodendrocytes and the axons they myelinate, we could suggest that both multiple sclerosis and schizophrenia may use in central nervous system a common pathway of disordered information-processing. Recent research suggests that adaptive myelination could normalize neuronal electrical excitability, which in turn can modify myelin plasticity, resulting to neural activity and behavior modulation. We may suggest that interventions that preserve white matter integrity or ameliorate white matter disruption may enhance information-processing and functional outcome in psychosis.
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