| Early diagnosis | Network changes may precede clinical symptoms |
| Disease staging | Connectivity patterns correlate with disease progression |
| Therapeutic targeting | Network hubs represent potential intervention points |
| Differential diagnosis | Distinct patterns help distinguish CBS from PSP and FTD |
| Seed-based connectivity | Examining connectivity from regions of interest (e.g., motor cortex, basal ganglia) |
| Independent Component Analysis (ICA) | Identifying intrinsic connectivity networks |
| Graph theoretical measures | Quantifying network topology (degree, betweenness, clustering) |
| Motor cortex hypo-connectivity | Reduced connectivity in the contralateral primary motor and premotor cortices |
| Premotor cortex dysfunction | Altered supplementary motor area (SMA) connectivity contributing to apraxia |
| Parietal association cortex | Reduced connectivity in the superior and inferior parietal lobules, correlating with cortical sensory loss |
| Sensorimotor circuit hypo-connectivity | Reduced communication between motor cortex and putamen/globus pallidus |
| Hyper-connectivity patterns | Compensatory increased connectivity in association loops |
| KG Connections | 1 knowledge graph edges |
| Databases | OMIMOrphanetClinicalTrialsPubMed |
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