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Published on: June 3, 2020
The degeneration changes of basal forebrain are associated with prospective memory impairment in patients with
Yutong Wu1, Sheng Hu1,2, Yi Wang1
1School of Medical Information Engineering, Anhui University of Chinese Medicine, Hefei, Anhui, China.
Introduction:
Degeneration changes of the basal forebrain (BF) are suggested to play an important role in cognitive impairment and memory loss in patients with Alzheimer's disease and Parkinson's disease. However, little is known about if and how the structure and function of BF are abnormal in Wilson's disease (WD).
Methods:
Here, we employed the structural and resting-state functional magnetic resonance imaging (fMRI) data from 19 WD individuals and 24 healthy controls (HC). Voxel-based morphometry (VBM) and functional connectivity analysis were applied to investigate the structural and functional degeneration changes of BF in WD. Moreover, the linear regression analyses were performed in the patient group to depict the correlations between the aberrant gray volume and functional connectivity of the BF and clinical performances, such as the prospective memory (PM) and mini-mental state examination (MMSE).
Results:
VBM analysis showed that compared with HC, the volume of overlapping cell groups of BF termed CH1-3 and CH4 was significantly reduced in WD. Additionally, the decreased functional connectivity of the CH4 was distributed in the bilateral temporal-parietal junction (TPJ), right thalamus, orbitofrontal gyrus (ORB), and left middle cingulate cortex (MCC). The performances of the time-based prospective memory (TBPM) and event-based prospective memory (EBPM) were related to reduced functional connectivity between CH4 and right ORB. Besides, the functional connectivity of left TPJ was also significantly correlated with EBPM in WD.
Conclusion:
These findings indicated that the degenerative changes of BF may affect PM through the innervation brain function and may help to understand the neural mechanisms underlying cognitive impairment in WD.
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