<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Beaud, Marie-Laure</dc:creator>
  <dc:creator>Rouiller, Eric M.</dc:creator>
  <dc:creator>Bloch, Jocelyne</dc:creator>
  <dc:creator>Mir, Anis</dc:creator>
  <dc:creator>Schwab, Martin E.</dc:creator>
  <dc:creator>Schmidlin, Eric</dc:creator>
  <dc:date>2019-08-16</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">In spinal cord injured adult mammals, neutralizing the neurite growth inhibitor Nogo‐A  with antibodies promotes axonal regeneration and functional recovery, although  axonal regeneration is limited in length. Neurotrophic factors such as BDNF stimulate  neurite outgrowth and protect axotomized neurons. Can the effects obtained by  neutralizing Nogo‐A, inducing an environment favorable for axonal sprouting, be  strengthened by adding BDNF? A unilateral incomplete hemicord lesion at C7 level  interrupted the main corticospinal component in three groups of adult macaque  monkeys: control monkeys (n = 6), anti‐Nogo‐A antibody‐treated monkeys (n = 7), and  anti‐Nogo‐A antibody and BDNF‐treated monkeys (n = 5). The functional recovery of  manual dexterity was significantly different between the 3 groups of monkeys, the  lowest in the control group. Whereas the anti‐Nogo‐A antibody‐treated animals  returned to manual dexterity performances close to prelesion ones, irrespective of  lesion size, both the control and the anti‐Nogo‐A/BDNF animals presented a limited  functional recovery. In the control group, the limited spontaneous functional recovery  depended on lesion size, a dependence absent in the combined treatment group  (anti‐Nogo‐A antibody and BDNF). The functional recovery in the latter group was  significantly lower than in anti‐Nogo‐A antibody‐treated monkeys, although the lesion  was larger in three out of the five monkeys in the combined treatment group.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://folia.unifr.ch/global/documents/308170</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/308170/files/rou_can.pdf</dc:identifier>
  <dc:identifier>https://folia.unifr.ch/documents/308170/files/rou_can_sm.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1111/cns.13213</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>License undefined</dc:rights>
  <dc:source>CNS Neuroscience &amp; Therapeutics. - 2019, p. cns.13213</dc:source>
  <dc:subject>info:eu-repo/classification/udc/57</dc:subject>
  <dc:title xmlns:ns1="xml" ns1:lang="en">Combined with anti‐Nogo‐A antibody treatment, BDNF did not compensate the extra deleterious motor effect caused by large size cervical cord hemisection in adult macaques</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>