Whether the underlying FTD molecular class can be identified by its impact on network-specific connectivity, however, remains unknown. Considering the role of anatomy (rather than the specific misfolded protein) in driving the clinical syndrome, there is reason to suspect that anatomically based methods (including resting-state network mapping) may struggle to reliably differentiate patients with bvFTD due to FTLD-tau vs. FTLD-TDP vs. FTLD-FUS, for example. On the other hand, it remains possible that to date bvFTD remains an overly inclusive clinical syndrome. If so, further clinical or anatomical differentiation may improve our ability to predict pathology during life.90,91
