@article{zhu2014spinal,
  title = {Spinal Cord Brain Derived Neurotrophic Factor (BDNF) Responsive Cells in an Experimental Autoimmune Encephalomyelitis (EAE) Model of Multiple Sclerosis (MS): Implications in Myelin Repair},
  author = {Wenjun Zhu and Crystal Acosta and Brian J. MacNeil and Thomas Klonisch and Claudia Cortes and Malcolm Doupe and Yuewen.Gong and Michael Namaka},
  year = 2014,
  url = {https://ibimapublishing.com/articles/IMMU/2014/612406/},
  journal = {Research in Immunology: An International Journal},
  volume = 2014 (2014),
  pages = 19,
  doi = 10.5171/2014.612406,
  abstract = {Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease that destroys central nervous system (CNS) myelin. Although, the exact pathophysiology of MS is unknown, it is associated with CNS infiltration of T-cells and monocytes, which subsequently activate phagocytic cells that directly damage myelin.  Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase receptor (TrkB), have recognized roles in myelin structure formation, maintenance, and repair. We used an experimental autoimmune encephalomyelitis (EAE) model of MS to determine changes in TrkB expression that may contribute to neurological recovery and myelin repair following an early inflammatory immune-mediated attack on CNS myelin. Spinal cord (SC) TrkB gene and protein expression were analyzed at various time intervals post-EAE induction. Analysis of gene and protein expression was conducted in animals with EAE relative to active controls (AC) and naïve controls (NC). We showed significant increases in TrkB protein in the SC of EAE rats 12 days post-induction relative to controls. This elevated TrkB expression correlated with the onset of neurological recovery days 12 to 15 post-EAE induction. Furthermore, immunohistochemistry (IHC) analysis revealed up-regulated expression of TrkB in several SC cell types including a specific subset of BDNF responsive neuronal cells. Finally, transmission electron microscopy (TEM) showed the ultrastructural integrity of myelin is already compromised during the early, inflammatory stage of EAE prior to widespread demyelination.  Therefore, the molecular signaling of SC BDNF via TrkB represents a key therapeutic target whose manipulation could facilitate myelin repair and neurological recovery following an MS-induced myelin attack.},
  keywords = {EAE; TrkB; spinal cord; multiple sclerosis},
  note = Article ID: 612406
}