Zinc as mediator of ubiquitin conjugation following Traumatic Brain Injury

I'm sure this might be important to us. Our researchers need to respond. If we had a Great stroke association this would be looked into.
http://www.sciencedirect.com/science/article/pii/S0006899313002035

Abstract

Previous studies have shown that pathological zinc accumulation and deposition of ubiquitinated protein aggregates are commonly detected in many acute neural injuries, such as trauma, epilepsy and ischemia, However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on ubiquitin conjugation and subsequent neurodegeration following traumatic brain injury (TBI). Firstly, we found that scavenging endogenous Zn²⁺ reduced trauma-induced ubiquitin conjugation and protected neurons from TBI insults in rat hippocampus. Secondly, we detected both zinc accumulation and increased ubiquitin conjugated protein following brain trauma in human cortical neurons. Our previous study has shown that zinc can induce ubiquitin conjugation in cultured hippocampal neurons. All these findings indicate that alterations in Zn²⁺ homeostasis may impair the protein degradation pathway and ultimately cause neuronal injury following traumatic brain injury.