Functional connectivity of cerebellar dentate nucleus and cognitive impairments in patients with drug-naive and first-episode schizophrenia.

• We were first to investigate the functional connectivity (FC) of cerebellar dentate nucleus (DN) with whole-brain and its association with cognitive impairments as well psychotic symptoms in patients with drug-naïve and first-episode schizophrenia. • The DN showed increased FC with the bilateral postcentral gyrus and decreased FC with the right inferior temporal gyrus and regional cerebellum (e.g., Vermis 4-5 and Crus I). • These abnormal DN FC correlated with cognitive impairments (e.g., working memory and processing speed) and symptom severity (e.g., negative symptom). Cognitive impairments are the hallmark of schizophrenia and prominent in the early episode stage. However, the underlying pathological mechanisms of cognitive impairments are not fully understood. This study aimed to investigate the abnormal functional connectivity (FC) of the cerebellar dentate nucleus (DN) and its correlation with cognitive impairments in patients with drug-naive and first-episode schizophrenia. Resting-state functional magnetic resonance imaging data were acquired in 47 patients and 43 healthy controls. Cognitive functions were assessed by number sequence span, verbal category fluency, digit-symbol coding tests. The results showed that the patients had deficits in all three cognitive tests compared to the controls. Furthermore, the increased FC of DN with the bilateral postcentral gyrus and decreased FC of DN with the right inferior temporal gyrus and regional cerebellum (e.g., Vermis 4-5 and Crus I) were observed in the patient group compared to the control group. Importantly, these abnormal DN FC significantly correlated with cognitive tests (e.g., number sequence span and digit-symbol coding) and clinical symptoms (e.g., negative symptom) in the patient group. The results suggested that abnormal FC of DN with cortical and subcortical regions was associated with cognitive impairments and symptom severity and might be an underlying neural mechanism in schizophrenia. [ABSTRACT FROM AUTHOR]