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To the Editor:
We read with interest the article by Salloway et al.,1 who describe a phase 2 ascending dose trial where bapineuzumab, a monoclonal antibody directed at the N-terminus of A beta, was tested in patients with Alzheimer disease (AD).
Although bapineuzumab did not affect the primary endpoint of cognitive outcome, APOE4 was associated with increased incidence of vasogenic edema. These results—along with other studies demonstrating an interaction between APOE polymorphism and treatment effect—highlight the importance of understanding pharmacogenomic interactions between APOE genotype and therapeutic strategies when designing future clinical trials.2
Since the original association was made between APOE genotype and risk of developing AD,3 there has been a strong focus on examining the isoform-specific effects of apoE on amyloid metabolism. Salloway et al. speculate that an increase in vascular amyloid burden may have resulted in vasogenic edema in APOE4 carriers. However, there are data suggesting that apoE modifies CNS inflammatory responses in an isoform-specific fashion; a potential common denominator for its role in acute and chronic neurologic diseases. …
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