The NAAG'ing Concerns of Modeling Human Alzheimer's Disease in Mice

Kristen Hollinger, Jesse Alt, Rana Rais, Adam I Kaplin, Barbara Slusher

Research output: Contribution to journalArticle


Studies over the past two decades report significant reductions in brain N-acetylaspartyl glutamate (NAAG) levels in neurodegenerative diseases with associated cognitive impairment, including Alzheimer's disease (AD). Because NAAG is cleaved by glutamate carboxypeptidase II (GCPII), restoration of brain NAAG levels via GCPII inhibition is a potential therapeutic strategy for AD. Herein, studies were conducted to identify an appropriate murine model of AD that recapitulates human brain NAAG changes in order to preclinically evaluate the therapeutic benefit of GCPII inhibition. Our opposing findings of brain NAAG changes in human and mouse AD highlights the limited predictive value of AD mouse models.

Original languageEnglish (US)
Pages (from-to)939-945
Number of pages7
JournalJournal of Alzheimer's Disease
Issue number3
StatePublished - Jan 1 2019


  • Alzheimer's disease
  • animal models
  • drug discovery
  • mass spectrometry

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

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