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Abnormal functional connectivity of the amygdala is associated with depressive symptoms in patients with multiple system atrophy

PURPOSE: Depressive symptoms are frequent nonmotor symptoms that occur in multiple system atrophy (MSA) patients. However, possible changes that can present in the amygdala (AMY) functional connectivity (FC) of the brain in MSA patients with depressive symptoms (DMSA patients) remain largely unknown...

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Detalles Bibliográficos
Autores principales: Zhao, Bin, Liu, Hu, Li, Huanhuan, Shang, Xiuli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6247974/
https://www.ncbi.nlm.nih.gov/pubmed/30532544
http://dx.doi.org/10.2147/NDT.S178657
Descripción
Sumario:PURPOSE: Depressive symptoms are frequent nonmotor symptoms that occur in multiple system atrophy (MSA) patients. However, possible changes that can present in the amygdala (AMY) functional connectivity (FC) of the brain in MSA patients with depressive symptoms (DMSA patients) remain largely unknown. MATERIALS AND METHODS: Resting-state functional magnetic resonance imaging scans were obtained from 29 DMSA patients, 28 MSA patients without depression symptoms (NDMSA patients), and 34 healthy controls (HCs). FC was analyzed by defining the bilateral AMY as the seed region. Correlation analysis was performed between the FC and clinical scores. RESULTS: When compared with NDMSA patients, DMSA patients showed increased bilateral AMY FC in the left middle frontal gyrus (MFG) and decreased right AMY FC in the left middle occipital gyrus. Moreover, the AMY FC values in the left middle frontal cortex were positively correlated with the Hamilton Depression Rating Scale-17 item scores. Furthermore, relative to the HCs, DMSA patients presented decreased bilateral AMY FC values in the visuospatial cortex, sensorimotor networks, and limbic areas. CONCLUSION: Depressive symptoms are associated with AMY–MFG FC anomalies in MSA patients. We propose that the middle frontal cortex may play an important role in the neuropathophysiology of depression in MSA patients.