Interfering with the Chronic Immune Response Rescues Chronic Degeneration After Traumatic Brain Injury
Ali Erturk, Susanne Mentz, Erik E. Stout, Maj Hedehus, Sara L. Dominguez, Lisa Neumaier, Franziska Krammer, Gemma Llovera, Karpagam Srinivasan, David V. Hansen, Arthur Liesz, Kimberly A. Scearce-Levie, and Morgan Sheng Contributed by Sloka S. Iyengar, PhD.
Contributed by Sloka Iyengar
Journal of Neuroscience 21 September 2016 36 (38) 9962-9975; DOI: 10.1523/JNEUROSCI.1898-15.2016
Acute changes as a result of TBI (e.g. apoptosis) are somewhat better understood; however long-term changes in the brain after an injury are still not well known. The focus of this paper is whether and how neurons that survive in the brain after an injury contribute to long-term deleterious effects. After the closed-head model of TBI, mice were shown to have tissue damage, a reduction in dendritic spine density, an increase in inflammation, and an increase in activation of microglia and astrocytes. These changes were widespread and persistent. Looking closely at the receptor for the chemokine fractalkine (CX3CR1), the authors found that deletion of one allele of CX3CR1 (in CX3CR1 -/- mice), protected mice from chronic neurodegeneration. This effect was more pronounced in female mice. Hence, the authors explored long-term effects of the initial injury in TBI, and found a potential target for a novel therapeutic strategy.
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