Abstract
ObjectiveThe objective of this study is to explore the brain activity alterations in Parkinson’s disease (PD) from the perspectives of neuronal activity, synchronization of neuronal activity, and coordination of whole-brain activity. MethodsIn this study, we recruited 38 PD patients and 35 matched healthy controls (HCs). We explored intrinsic brain activity alterations in PD by comparing resting-state functional magnetic resonance imaging (rs-fMRI) metrics of the amplitude of low-frequency of fluctuation (ALFF), the fractional amplitude of low-frequency fluctuation (fALFF), percent amplitude of fluctuation (PerAF), regional homogeneity (ReHo), and degree centrality (DC). Two-sample t-tests were used to determine the differences between the two groups. Spearman correlation analysis was used to explore the relationships between abnormal ALFF, fALFF, PerAF, ReHo, and DC values and clinical indicators such as the Movement Disorder Society’s Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), Hoehn and Yahr (H&Y) stage, and duration of disease. ResultsCompared with the HCs, PD had increased ALFF,fALFF, and PerAF in the temporal lobe and cerebellum, and decreased ALFF,fALFF, and PerAF in the occipital-parietal lobe in the neuronal activity. In the synchronization of neuronal activity, PD patients had increased ReHo in the right inferior parietal lobule and decreased ReHo in the caudate. In the coordination of whole-brain activity, PD patients had increased DC in the cerebellum and decreased DC in the occipital lobe. Correlation analysis showed that there is a correlation between abnormal brain regions and clinical indicators in PD. Notably, the changes in occipital lobe brain activity were found in ALFF, fALFF, PerAF, and DC, and were most correlated with the clinical indicators of PD patients. ConclusionsThis study found that intrinsic brain function in several occipital-temporal-parietal and cerebellum regions was altered in PD patients, potentially related to the clinical indicators of PD. These results may enhance our understanding of the underlying neural mechanisms of PD and may contribute to further exploring the selection of therapeutic targets in PD patients.
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