4.6 Article

Common and distinct roles of amygdala subregional functional connectivity in non-motor symptoms of Parkinson's disease

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NPJ PARKINSONS DISEASE
卷 9, 期 1, 页码 -

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NATURE PORTFOLIO
DOI: 10.1038/s41531-023-00469-1

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Neuroimaging studies have shown that dysfunction of the amygdala plays a crucial role in the non-motor symptoms of Parkinson's disease. However, the specific relationship between amygdala subregions and these symptoms has not been well-defined. Using resting-state functional MRI, researchers found that the amygdala subregions in Parkinson's disease exhibited altered functional connectivity, particularly with the frontal, temporal, insular cortex, and putamen. Each subregion also displayed distinct hypoconnectivity with different limbic systems, and this hypoconnectivity was associated with various non-motor symptoms such as emotion, pain, olfaction, cognition, and sleepiness. These findings provide new insights into the pathogenesis of non-motor symptoms in Parkinson's disease.
Neuroimaging studies suggest a pivotal role of amygdala dysfunction in non-motor symptoms (NMS) of Parkinson's disease (PD). However, the relationship between amygdala subregions (the centromedial (CMA), basolateral (BLA) and superficial amygdala (SFA)) and NMS has not been delineated. We used resting-state functional MRI to examine the PD-related alterations in functional connectivity for amygdala subregions. The left three subregions and right BLA exhibited between-group differences, and were commonly hypo-connected with the frontal, temporal, insular cortex, and putamen in PD. Each subregion displayed distinct hypoconnectivity with the limbic systems. Partial least-squares analysis revealed distinct amygdala subregional involvement in diverse NMS. Hypo-connectivity of all four subregions was associated with emotion, pain, olfaction, and cognition. Hypo-connectivity of the left SFA was associated with sleepiness. Our findings highlight the hypofunction of the amygdala subregions in PD and their preliminary associations with NMS, providing new insights into the pathogenesis of NMS.

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