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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Apolipoprotein E protects against NMDA excitotoxicity.

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.[1]

References

  1. Apolipoprotein E protects against NMDA excitotoxicity. Aono, M., Lee, Y., Grant, E.R., Zivin, R.A., Pearlstein, R.D., Warner, D.S., Bennett, E.R., Laskowitz, D.T. Neurobiol. Dis. (2002) [Pubmed]
 
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