Abstract

Traumatic brain injury (TBI), as a common disease, usually causes neurological damage, such as cognitive impairments, motor deficits, and neuropsychiatric deficits. As TBI occurs, a cascade reaction in the cellular and molecular levels will cause secondary damage, leading to the apoptosis of neurons and glial cells as well as brain edema, etc. However, the treatment is far from satisfaction owning to the complicated set of factors or pathways that are initiated post‐injury. As a bifunctional axonal guidance cue, netrin‐1 can attract axons via the deleted in colorectal cancer (DCC) receptors and repelling others via Unc5 receptors, but its exact role in the recovery of motor and sensory function after TBI has not well been studied, and the mechanisms remain elusive. Here, collecting the current literatures, we aimed to summarize and predict the exact role of netrin‐1 in TBI.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call