The onset of schizophrenia is often preceded by a prodromal phase, characterized by attenuated psychotic symptoms and functional impairment. Persons who meet the standardized criteria for this phase are at ultra-high risk for the development of a psychotic disorder. Effective, early intervention during this phase may forestall the onset of a fulminant psychotic disorder. However, it is difficult to “spot” schizophrenia in its earliest stages: only about 35% of high-risk persons will develop a psychotic disorder, primarily schizophrenia, within 24 months.1
There is increasing evidence that immune system dysfunction, including inflammation, may be present in persons at high risk for psychosis and may play a role in the pathophysiology of some patients with schizophrenia. Microglia—the resident immune cells in the central nervous system—may have abnormal activity and density in schizophrenia. Microglial activity can be measured in vivo with positron emission tomography (PET) using radioligands specific for the translocator protein (TSPO), which is expressed on microglia.
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