% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Klein:825262,
      author       = {Klein, Rebecca and Mahlberg, Nicolas and Ohren, Maurice and
                      Ladwig, Anne and Neumaier, Bernd and Graf, Rudolf and Hoehn,
                      Mathias and Albrechtsen, Morten and Rees, Stephen and Fink,
                      Gereon Rudolf and Rueger, Maria Adele and Schroeter,
                      Michael},
      title        = {{T}he {N}eural {C}ell {A}dhesion {M}olecule-{D}erived
                      ({NCAM})-{P}eptide {FG} {L}oop ({FGL}) {M}obilizes
                      {E}ndogenous {N}eural {S}tem {C}ells and {P}romotes
                      {E}ndogenous {R}egenerative {C}apacity after {S}troke},
      journal      = {Journal of neuroImmune pharmacology},
      volume       = {11},
      number       = {4},
      issn         = {1557-1904},
      address      = {Boston, MA [u.a.]},
      publisher    = {Springer},
      reportid     = {FZJ-2016-07733},
      pages        = {708 - 720},
      year         = {2016},
      abstract     = {The neural cell adhesion molecule (NCAM)-derived peptide FG
                      loop (FGL) modulates synaptogenesis, neurogenesis, and stem
                      cell proliferation, enhances cognitive capacities, and
                      conveys neuroprotection after stroke. Here we investigated
                      the effect of subcutaneously injected FGL on cellular
                      compartments affected by degeneration and regeneration after
                      stroke due to middle cerebral artery occlusion (MCAO),
                      namely endogenous neural stem cells (NSC), oligodendrocytes,
                      and microglia. In addition to immunohistochemistry, we used
                      non-invasive positron emission tomography (PET) imaging with
                      the tracer [18F]-fluoro-L-thymidine ([18F]FLT) to visualize
                      endogenous NSC in vivo. FGL significantly increased
                      endogenous NSC mobilization in the neurogenic niches as
                      evidenced by in vivo and ex vivo methods, and it induced
                      remyelination. Moreover, FGL affected neuroinflammation.
                      Extending previous in vitro results, our data show that the
                      NCAM mimetic peptide FGL mobilizes endogenous NSC after
                      focal ischemia and enhances regeneration by amplifying
                      remyelination and modulating neuroinflammation via affecting
                      microglia. Results suggest FGL as a promising candidate to
                      promote recovery after stroke.},
      cin          = {INM-5 / INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-5-20090406 / I:(DE-Juel1)INM-3-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000387362000010},
      pubmed       = {pmid:27352075},
      doi          = {10.1007/s11481-016-9694-5},
      url          = {https://juser.fz-juelich.de/record/825262},
}