Does an Alzheimer's disease susceptibility gene influence the cognitive effects of cancer therapy?

Authors

  • Richard J. Caselli MD

    Corresponding author
    1. Department of Neurology, Mayo Clinic, Scottsdale, Arizona
    2. Associate Director, Arizona Alzheimer's Disease Center, Scottsdale, Arizona
    • Correspondence to: Richard J. Caselli, Department of Neurology, Mayo Clinic Arizona, 13400 East Shea Blvd, Scottsdale, AZ 85259.

      E-mail: caselli.richard@mayo.edu

    Search for more papers by this author
    • Dr. Caselli affirms that he has no affiliations that he considers to be relevant and important with any organization that to his knowledge has a direct interest, particularly a financial interest, in the subject matter discussed. Such affiliations include, but are not limited to, employment by an industrial concern, ownership of stock, membership on a standing advisory council or committee, a seat on the board of directors, or being publicly associated with a company or its products.

Abstract

The apolipoprotein E (APOE) e4 allele is the most prevalent genetic risk factor for Alzheimer's disease (AD). APOE e4 carriers suffer greater morbidity from head trauma, stroke, and carbon monoxide poisoning, yet possible interactions between APOE genotype and cancer therapy on cognition are unclear. Neuropathological and biomarker studies of young asymptomatic APOE e4 carriers that show elevated neocortical amyloid and medial temporal neurofibrillary tangles and longitudinal neuropsychological studies that show accelerated memory decline beginning around age 55–60 years define preclinical AD and have set the stage for assessing the potential adverse cognitive effects of cancer therapy in APOE e4 carriers. Pediatr Blood Cancer 2014; 61:1739–1742. © 2013 Wiley Periodicals, Inc.

Ancillary