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@ARTICLE{Costa:284090,
      author       = {Costa, Vivian V. and Del Sarto, Juliana L. and Rocha,
                      Rebeca F. and Silva, Flavia R. and Doria, Juliana G. and
                      Olmo, Isabella G. and Marques, Rafael E. and Queiroz-Junior,
                      Celso M. and Foureaux, Giselle and Araújo, Julia Maria S.
                      and Cramer, Allysson and Real, Ana Luíza C. V. and Secchim
                      Ribeiro, Lucas and Sardi, Silvia I. and Ferreira, Anderson
                      J. and Machado, Fabiana S. and de Oliveira, Antônio C. and
                      Teixeira, Antônio L. and Nakaya, Helder I. and Souza,
                      Danielle G. and Ribeiro, Fabiola M. and Teixeira, Mauro M.},
      title        = {{N} -{M}ethyl- d -{A}spartate ({NMDA}) {R}eceptor
                      {B}lockade {P}revents {N}euronal {D}eath {I}nduced by {Z}ika
                      {V}irus {I}nfection},
      journal      = {mBio},
      volume       = {8},
      number       = {2},
      issn         = {2161-2129},
      address      = {Washington, DC},
      publisher    = {American Society for Microbiology},
      reportid     = {DZNE-2026-00098},
      pages        = {e00350-17},
      year         = {2017},
      abstract     = {Zika virus (ZIKV) infection is a global health emergency
                      that causes significant neurodegeneration. Neurodegenerative
                      processes may be exacerbated by N-methyl-d-aspartate
                      receptor (NMDAR)-dependent neuronal excitoxicity. Here, we
                      have exploited the hypothesis that ZIKV-induced
                      neurodegeneration can be rescued by blocking NMDA
                      overstimulation with memantine. Our results show that ZIKV
                      actively replicates in primary neurons and that virus
                      replication is directly associated with massive neuronal
                      cell death. Interestingly, treatment with memantine or other
                      NMDAR blockers, including dizocilpine (MK-801), agmatine
                      sulfate, or ifenprodil, prevents neuronal death without
                      interfering with the ability of ZIKV to replicate in these
                      cells. Moreover, in vivo experiments demonstrate that
                      therapeutic memantine treatment prevents the increase of
                      intraocular pressure (IOP) induced by infection and
                      massively reduces neurodegeneration and microgliosis in the
                      brain of infected mice. Our results indicate that the
                      blockade of NMDARs by memantine provides potent
                      neuroprotective effects against ZIKV-induced neuronal
                      damage, suggesting it could be a viable treatment for
                      patients at risk for ZIKV infection-induced
                      neurodegeneration.IMPORTANCE Zika virus (ZIKV) infection is
                      a global health emergency associated with serious
                      neurological complications, including microcephaly and
                      Guillain-Barré syndrome. Infection of experimental animals
                      with ZIKV causes significant neuronal damage and
                      microgliosis. Treatment with drugs that block NMDARs
                      prevented neuronal damage both in vitro and in vivo These
                      results suggest that overactivation of NMDARs contributes
                      significantly to the neuronal damage induced by ZIKV
                      infection, and this is amenable to inhibition by drug
                      treatment.},
      keywords     = {Animals / Disease Models, Animal / Mice / Neurodegenerative
                      Diseases: drug therapy / Neurodegenerative Diseases:
                      pathology / Neuroprotective Agents: administration $\&$
                      dosage / Receptors, N-Methyl-D-Aspartate: antagonists $\&$
                      inhibitors / Treatment Outcome / Zika Virus: growth $\&$
                      development / Zika Virus Infection: complications / Zika
                      Virus Infection: pathology / NMDA receptor (Other) / Zika
                      virus (Other) / intraocular pressure (Other) / memantine
                      (Other) / microgliosis (Other) / mouse model (Other) /
                      neuronal death (Other) / Neuroprotective Agents (NLM
                      Chemicals) / Receptors, N-Methyl-D-Aspartate (NLM
                      Chemicals)},
      ddc          = {570},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1128/mBio.00350-17},
      url          = {https://pub.dzne.de/record/284090},
}