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Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
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Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
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Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype

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Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype
Journal Article

Fine‐grained features characterize hippocampal and amygdaloid change pattern in Parkinson's disease and discriminate cognitive‐deficit subtype

2024
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Overview
Aims To extract vertex‐wise features of the hippocampus and amygdala in Parkinson's disease (PD) with mild cognitive impairment (MCI) and normal cognition (NC) and further evaluate their discriminatory efficacy. Methods High‐resolution 3D‐T1 data were collected from 68 PD‐MCI, 211 PD‐NC, and 100 matched healthy controls (HC). Surface geometric features were captured using surface conformal representation, and surfaces were registered to a common template using fluid registration. The statistical tests were performed to detect differences between groups. The disease‐discriminatory ability of features was also tested in the ensemble classifiers. Results The amygdala, not the hippocampus, showed significant overall differences among the groups. Compared with PD‐NC, the right amygdala in MCI patients showed expansion (anterior cortical, anterior amygdaloid, and accessory basal areas) and atrophy (basolateral ventromedial area) subregions. There was notable atrophy in the right CA1 and hippocampal subiculum of PD‐MCI. The accuracy of classifiers with multivariate morphometry statistics as features exceeded 85%. Conclusion PD‐MCI is associated with multiscale morphological changes in the amygdala, as well as subtle atrophy in the hippocampus. These novel metrics demonstrated the potential to serve as biomarkers for PD‐MCI diagnosis. Overall, these findings from this study help understand the role of subcortical structures in the neuropathological mechanisms of PD cognitive impairment. We introduced a conformal representation method to calculate vertex‐wise features in the hippocampus and amygdala in PD‐MCI and PD‐NC. Compared with PD‐NC, the amygdala of PD‐MCI showed both global and subfields' alterations (expanded anterior cortical, anterior amygdaloid, and accessory basal areas and atrophied basolateral ventromedial area), with only atrophy found in the right hippocampal subiculum. The novel features from the above regions achieved accuracy exceeding 85% in classification tasks.