The efficacy of an anti-nerve growth factor (NGF) antibody in preventing rearrangements of whole-brain functional connectivity elicited by nociceptive input following bone metastases was evaluated in a mouse model of cancer-induced bone pain using longitudinal resting-state fMRI. ROI-based network and seed-based connectivity analysis approaches revealed major hubs of ascending and descending pain pathways to be affected by the developing pain. Functional rearrangements within these regions could be prevented by prospective application of anti-NGF antibody mAb911 indicating the efficacy of anti-NGF treatment in preventing, or at least delaying, adaptations of the brain circuitry associated with development of a chronic pain state.
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