A fascinating read I just found out about via Twitter: http://www.alzforum.org/news/conference-coverage/traumatic-brain-injury-focus-heterogeneity-secondary-damage
From the text (emphasis is mine):
TBI Beyond Tau
Overall, few of the talks at SfN focused on tau, instead highlighting other aspects of brain damage. Michal Vascak in John Povlishock’s group at Virginia Commonwealth University, Richmond, detailed what happens to axons after brain injury. Vascak used a model of mild TBI in which a device rapidly injects a small volume of saline into a mouse brain, subjecting cells to a fluid concussion wave. This does not cause brain lesions or hemorrhages, but a diffuse, widespread axonal injury ensues as fragile neuronal connections twist and shear around the injury site. Moreover, even those axons that do not break may be affected, Vascak said. He reported that two days after injury, intact axons did not fire properly. He wondered if this might be due to changes in the axon initial segments, where action potentials are generated.
To get a closer look at those segments, Vascak used confocal microscopy to image individual uninjured axons in postmortem mouse brain two days after injury. Using specific markers to identify the ends of initial segments, he found that the distal end had shrunk by about 2 μm. Since this end triggers action potentials, the change would alter neuronal firing properties, and that in turn might affect overall network excitability, Vascak suggested. The data demonstrate that TBI can affect the properties of even intact axons.
Read the full article here: : http://www.alzforum.org/news/conference-coverage/traumatic-brain-injury-focus-heterogeneity-secondary-damage