Apolipoprotein E protects against NMDA excitotoxicity

Mitsuo Aono, Yoonki Lee, Elfrida R. Grant, Robert A. Zivin, Robert D. Pearlstein, David S. Warner, Ellen R. Bennett, Daniel T. Laskowitz

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Preclinical and clinical evidence implicates a role for endogenous apolipoprotein E in modifying the response of the brain to focal and global ischemia. To investigate whether apoE modulates the neuronal response to glutamate excitotoxicity, we exposed primary neuronal glial cultures and a neuronal cell line to biologically relevant concentrations of apolipoprotein E prior to NMDA exposure. In both of these paradigms, apolipoprotein E exerted partial protective effects. At neuroprotective concentrations, however, apolipoprotein E failed to block NMDA-induced calcium influx to the same magnitude as the NMDA receptor antagonist MK-801. These results suggest that one mechanism by which apolipoprotein E modifies the central nervous system response to ischemia may be by reducing glutamate-induced excitotoxicity.

Original languageEnglish (US)
Pages (from-to)214-220
Number of pages7
JournalNeurobiology of Disease
Issue number1
StatePublished - 2002
Externally publishedYes


  • Apolipoprotein E
  • Calcium influx
  • Cell culture
  • Cerebral ischemia
  • Excitotoxicity
  • Neuroprotection
  • NMDA
  • RAP

ASJC Scopus subject areas

  • Neurology


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