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Editorial
October 2014

Is Apolipoprotein E Required for Cognitive Function in Humans?Implications for Alzheimer Drug Development

Author Affiliations
  • 1Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas
  • 2Center for Alzheimer’s and Neurodegenerative Diseases, University of Texas Southwestern Medical Center, Dallas
  • 3Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas
  • 4Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas
JAMA Neurol. 2014;71(10):1213-1215. doi:10.1001/jamaneurol.2014.2013

More than 20 years ago, a polymorphism in the apolipoprotein E (apoE) gene was identified as the primary risk factor for late-onset Alzheimer disease (AD).1 Individuals carrying the ε4 isoform of apoE (apoE4) are at significantly greater risk for AD compared with apoE3 carriers, whereas the apoE2 allele is associated with reduced AD risk.2 Despite 2 decades of research into the mechanisms by which apoE4 contributes to disease pathogenesis, a seemingly simple question remains unresolved: is apoE good or bad for brain health? The answer to this question is essential for the future development of apoE-directed therapeutics.

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