Abstract
Many clinical symptoms of sporadic Parkinson’s disease (sPD) cannot be completely explained by a lesion of the simple typical extrapyramidal circuit between the striatum and substantia nigra. Therefore, this study aimed to explore the new potential damaged pathogenesis of other brain regions associated with the multiple and complex clinical symptoms of sPD through magnetic resonance imaging (MRI). A total of 65 patients with mid-stage sPD and 35 healthy controls were recruited in this study. Cortical structural connectivity was assessed by seed-based analysis using the vertex-based morphology of MRI. Seven different clusters in the brain regions of cortical thickness thinning derived from the regression analysis using brain size as covariates between sPD and control were selected as seeds. Results showed that the significant alteration of cortical structural connectivity mainly occurred in the bilateral frontal orbital, opercular, triangular, precentral, rectus, supplementary-motor, temporal pole, angular, Heschl, parietal, supramarginal, postcentral, precuneus, occipital, lingual, cuneus, Rolandic-opercular, cingulum, parahippocampal, calcarine, olfactory, insula, paracentral-lobule, and fusiform regions at the mid-stage of sPD. These findings suggested that the extensive alteration of cortical structural connectivity is one of possible pathogenesis resulting in the multiple and complex clinical symptoms in sPD.
Highlights
Sporadic Parkinson’s disease is a neurodegenerative disorder, it is mainly caused by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta projecting to the striatum
The brain regions of thinning thickness in the regression analysis using brain size as a covariate were used as the chosen seeds, according to information from 47 seed-based correlation analyses (SCA) regarding structural covariates, cortical structural connectivity between the chosen brain regions was analyzed using the voxel-based morphometry (VBM) of magnetic resonance imaging (MRI) (Supplementary Table 1 and Figures 1–7A)
Results revealed that an extensive alteration in cortical structural connectivity occurred in mid-stage Sporadic Parkinson’s disease (sPD) patients, the brain regions of abnormal cortical structural connectivity in the mid-stage sPD patients versus the controls are summarized in Supplementary Tables 3–9
Summary
Sporadic Parkinson’s disease (sPD) is a neurodegenerative disorder, it is mainly caused by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta projecting to the striatum. The damage of substantia nigra-striatum loops is believed to lead to the hallmarked motor dysfunctions of sPD including tremors, rigidity, bradykinesia, and postural instability (Jankovic, 2008; Göttlich et al, 2013). Cortical Structural Connectivity Alterations in sPD brain functions has been found in the different stages of sPD. These functional deficits in these brain regions result in multiple and complex clinical symptoms in sPD, which include behavioral disorders, cognitive dysfunction, and autonomic dysfunction such as orthostatic symptoms, incontinence, constipation, hyposmia, and/or dyssomnia (Göttlich et al, 2013; Khoo et al, 2013). The relational pathogenesis of brain area damage associated with these multiple and complex clinical symptoms of sPD still remains unclear
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