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@ARTICLE{Varbanov:257594,
      author       = {Varbanov, Hristo and Jia, Shaobo and Kochlamazashvili, Gaga
                      and Bhattacharya, Subhrajit and Buabeid, Manal Ali and El
                      Tabbal, Mohamed and Hayani, Hussam and Stoyanov, Stoyan and
                      Sun, Weilun and Thiesler, Hauke and Röckle, Iris and
                      Hildebrandt, Herbert and Senkov, Oleg and Suppiramaniam,
                      Vishnu and Gerardy-Schahn, Rita and Dityatev, Alexander},
      title        = {{R}escue of synaptic and cognitive functions in polysialic
                      acid-deficient mice and dementia models by short polysialic
                      acid fragments.},
      journal      = {Neurobiology of disease},
      volume       = {180},
      issn         = {0969-9961},
      address      = {[Amsterdam]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-00470},
      pages        = {106079},
      year         = {2023},
      abstract     = {Dysregulated cortical expression of the neural cell
                      adhesion molecule (NCAM) and deficits of its associated
                      polysialic acid (polySia) have been found in Alzheimer's
                      disease and schizophrenia. However, the functional role of
                      polySia in cortical synaptic plasticity remains poorly
                      understood. Here, we show that acute enzymatic removal of
                      polySia in medial prefrontal cortex (mPFC) slices leads to
                      increased transmission mediated by the GluN1/GluN2B subtype
                      of N-methyl-d-aspartate receptors (NMDARs), increased
                      NMDAR-mediated extrasynaptic tonic currents, and impaired
                      long-term potentiation (LTP). The latter could be fully
                      rescued by pharmacological suppression of GluN1/GluN2B
                      receptors, or by application of short soluble polySia
                      fragments that inhibited opening of GluN1/GluN2B channels.
                      These treatments and augmentation of synaptic NMDARs with
                      the glycine transporter type 1 (GlyT1) inhibitor sarcosine
                      also restored LTP in mice deficient in polysialyltransferase
                      ST8SIA4. Furthermore, the impaired performance of
                      polySia-deficient mice and two models of Alzheimer's disease
                      in the mPFC-dependent cognitive tasks could be rescued by
                      intranasal administration of polySia fragments. Our data
                      demonstrate the essential role of polySia-NCAM in the
                      balancing of signaling through synaptic/extrasynaptic NMDARs
                      in mPFC and highlight the therapeutic potential of short
                      polySia fragments to restrain GluN1/GluN2B-mediated
                      signaling.},
      keywords     = {Mice / Animals / Alzheimer Disease: drug therapy / Sialic
                      Acids: metabolism / Cognition / Neural Cell Adhesion
                      Molecules: metabolism / Receptors, N-Methyl-D-Aspartate /
                      NCAM (Other) / NMDA receptor (Other) / Polysialic acid
                      (Other) / Prefrontal cortex (Other) / Synaptic plasticity
                      (Other) / polysialic acid (NLM Chemicals) / Sialic Acids
                      (NLM Chemicals) / Neural Cell Adhesion Molecules (NLM
                      Chemicals) / Receptors, N-Methyl-D-Aspartate (NLM
                      Chemicals)},
      cin          = {AG Dityatev},
      ddc          = {570},
      cid          = {I:(DE-2719)1310007},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36918046},
      doi          = {10.1016/j.nbd.2023.106079},
      url          = {https://pub.dzne.de/record/257594},
}