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Significance Growing evidence from in vitro studies suggests that the axonal cytoskeleton plays a mechanoprotective role in axon while under dynamic mechanical loads during a traumatic brain injury (TBI). Via computational modeling, we elucidate how perturbations in physical properties of the salient components of axonal cytoskeleton impact the intraaxonal load-bearing mechanism, potentially resulting in its failure. Immunohistochemical analyses of tissue from an in vivo model of TBI confirm the presence of cytoskeletal neurochemical degradation. In conjunction with the experiments, our model explains the clinical observation of exacerbated axonal pathology after repetitive TBIs. Insights from this work can help advance the understanding of the long-term impacts of single and repeated TBIs and identify potential therapeutic targets for improving axonal response to injury.

Modeling links softening of myelin and spectrin scaffolds of axons after a concussion to increased vulnerability to repeated injuries