| Autor: |
Briels, Casper T., Eertink, J.J., Stam, Cornelis J., van Der Flier, Wiesje, Scheltens, Philip, Gouw, Alida A. |
| Zdroj: |
Alzheimer's & Dementia: The Journal of the Alzheimer's Association; Dec2020 Supplement S11, Vol. 16 Issue 11, p1-3, 3p |
| Abstrakt: |
Background: Electroencephalography (EEG) has shown differences in spectral, functional connectivity and network measures between typical Alzheimer's disease (AD) and controls. Subjects with posterior cortical atrophy (PCA) show more severe visuospatial and perceptual deficits compared to typical AD. The aim of this study was to investigate whether functional alterations measured by EEG can help understand the mechanisms that explain the clinical heterogeneity. Methods: 21‐channel EEG recordings of 29 PCA subjects, with positive biomarkers for amyloid pathology, were compared with 29 typical AD subjects and 29 controls with subjective cognitive decline matched for age, gender and disease duration (respectively 41%/38%/45% male, age:63±5/63±5/63±5yr, median MMSE:19/18/28). Relative band power, alpha band functional connectivity (defined by volume conduction corrected amplitude envelope correlation) and network characteristics of the minimum spanning tree(MST) were assessed at global and electrode levels. Differences between diagnostic groups were analysed with pairwise permutation testing. Correlations between electrode level peak frequency with visual (dotcounting and fragmented letters) and memory (Rey Auditory Verbal Learning Test) tasks were assessed within the PCA group. Results: PCA and AD subjects had a lower global relative alpha and beta and higher theta power compared to controls (p<0.05). PCA subjects had higher global relative delta and lower alpha power compared to AD subjects (p<0.05), driven by a decrease in the dominant posterior frequency (Figure 1). Global functional connectivity was decreased in both PCA and AD compared to controls (both p<0.001). The MST showed an increased network diameter, a decreased posterior and an increased frontal degree in PCA compared to controls (Figure 2). In PCA, decreased right posterior peak frequency correlated with worse performance on visual tasks (Dotcounting: r=0.50, p=0.012; fragmented letters: r=0.51, p=0.008) but not with the memory task (Figure 3). Conclusion: The clinical differences between PCA and typical AD subjects corresponded with a more severe slowing of oscillatory activity in the posterior regions in PCA subjects. The network of PCA subjects showed a less efficient topology and a shift in hubness from posterior to frontal channels. This indicates that in PCA, regional synaptic dysfunction might interplay with previously reported atrophy and tau accumulation in the networks responsible for visual processing. [ABSTRACT FROM AUTHOR] |
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