Emergent Functional Network Effects in Parkinson Disease
| Autor: | Baijayanta Maiti, Deanna J. Greene, Jonathan M. Koller, Meghan C. Campbell, Joel S. Perlmutter, William D. Shannon, Caterina Gratton, Abraham Z. Snyder, Steven E. Petersen |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Male
Cognitive Neuroscience Disease Biology 050105 experimental psychology Functional networks 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Group differences Neural Pathways medicine Connectome Humans 0501 psychology and cognitive sciences Aged business.industry Functional connectivity 05 social sciences Brain Parkinson Disease Original Articles Caudal brainstem Middle Aged Magnetic Resonance Imaging Pathophysiology medicine.anatomical_structure Cerebral cortex Female business Corrigendum Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Cereb Cortex |
| Popis: | The hallmark pathology underlying Parkinson disease (PD) is progressive synucleinopathy, beginning in caudal brainstem that later spreads rostrally. However, the primarily subcortical pathology fails to account for the wide spectrum of clinical manifestations in PD. To reconcile these observations, resting-state functional connectivity (FC) can be used to examine dysfunction across distributed brain networks. We measured FC in a large, single-site study of nondemented PD (N = 107; OFF medications) and healthy controls (N = 46) incorporating rigorous quality control measures and comprehensive sampling of cortical, subcortical and cerebellar regions. We employed novel statistical approaches to determine group differences across the entire connectome, at the network-level, and for select brain regions. Group differences respected well-characterized network delineations producing a striking “block-wise” pattern of network-to-network effects. Surprisingly, these results demonstrate that the greatest FC differences involve sensorimotor, thalamic, and cerebellar networks, with notably smaller striatal effects. Split-half replication demonstrates the robustness of these results. Finally, block-wise FC correlations with behavior suggest that FC disruptions may contribute to clinical manifestations in PD. Overall, these results indicate a concerted breakdown of functional network interactions, remote from primary pathophysiology, and suggest that FC deficits in PD are related to emergent network-level phenomena rather than focal pathology. |
| Databáze: | OpenAIRE |
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