http://linkinghub.elsevier.com/retrieve/pii/S0889159116302471?via=sd&cc=y
Brain, Behavior, and Immunity, Volume 57, Issue null, Page e15
F. Walker, K. Jones, Z. Zhao, L.K. Ong, M. Kluge, K. Zalewska, S. Johnson, M. Nilsson
Abstract
As our population ages stroke is becoming an ever more prevalent condition, afflicting tens of thousands of people(Totally wrong - millions yearly) every year. The initial stroke event results in a very significant loss of brain tissue at the site of infarction. Unfortunately, however, viable brain tissue continues to be lost after the primary infarction process is complete, in a process known as secondary neurodegeneration (SND)(neuronal cascade of death). SND involves the progressive death of brain regions that were connected to the original infarcted territories. To better understand SND we have developed a highly controllable model of SND. Specifically, we induce a small stroke within the somatosensory cortex with the assistance of a custom built intrinsic optical signal imaging tandem lens macroscope. This procedure initiates a tightly constrained SND process. We have identified that SND-linked neuroinflammatory disturbances spread out from the injury site, as indicated by significantly enhanced pro-inflammatory signalling (mRNA and protein levels), microglial morphology, neuronal loss (histology), and infiltration of peripheral immune cells (flow cytometry). We have identified that these events are significantly suppressed by chronic stress, or by corticosterone alone, which is in-turn associated with greater cell loss at sites of SND. Collectively, these results suggest that detailed monitoring of stress loads and stress reduction strategies may be warranted in patients recovering from stroke.
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