Presenilin1 familial Alzheimer disease mutants inactivate EFNB1- and BDNF-dependent neuroprotection against excitotoxicity by affecting neuroprotective complexes of <i>N</i>-methyl-d-aspartate receptor.

However, the increase in the GLUN1 association with PS1 mutants compared to WT proteins failed to reach significance due to variations associated with the overexpressions of WT and mutant proteins ( Supplementary Fig. 5 , right panel).

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While both WT and mutant PS1 associated with GLUN1, we observed a clear trend of mutant PS1 being associated more with GLUN1 ( Supplementary Fig. 5 , left upper panel).

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