抽象的

Relevance of exosomes with structural changes of white matter and cognitive impairment in patients with PD

Kai Chen, Xue-ning Zhang

Objective: To investigate the relevance of exosomes with structural changes of white matter and cognitive impairment in patients with Parkinson’s Disease (PD).

Methods: 60 patients with PD were selected between January 2013 and December 2015. All patients were divided into 3 groups according to their cognitive function: PD-N group, PD-M group and PDD group. General characteristics were collected and analysed. The movement functions of PD patients were evaluated by the UPDRS and Hoehn-Yahr (modified) rating scale. Patients with cognitive impairment were evaluated with the MMSE and the MoCA. The GE 3.0 T MRI was used for examination. All the cases were scanned with routine MRI sequence and Diffusion Tensor Imaging (DTI) sequence. Fractional Anisotropy (FA) was measured for white matter nerve fibers of different brain regions of interest. The serum levels of TNF-α and α-synuclein were measured by ELISA.

Results: The UPDRS and Hoehn-Yahr scale of PD increased gradually with the exacerbation of cognitive impairment (P<0.05). The proportion of Parkinson’s dementia in the middle and late group was significantly higher than that in the early group (P<0.05), while the proportion of the middle and late group with cognitive function was significantly lower than that of the early group (P<0.05). 21 out of 36 patients with normal MMSE scores had abnormal MoCA scores. Logistic regression analysis showing that the corpus callosum may be specific for the brain white matter; and so did the left temporal lobe and corpus callosum knee. The spearman correlation analysis showed that there was a negative correlation between regional brain white matter and Parkinson’s cognitive function. The levels of TNF-α and α-synuclein in the PD group were significantly higher than those in the normal control group (P<0.05).

Conclusion: There should be a certain relationship between serum exosomes containing α-synuclein and cognitive impairment in PD.