Various groups have explored the effect of apolipoprotein E (APOE) on neurodegeneration through nutritional and metabolic alterations. In this review, we hope to summarize recent findings in humans as well as preclinical APOE models.
Metabolic pathways including lipid metabolism appear to play a large role in the pathophysiology of Alzheimer's disease. Carrier status of the E4 variant of the APOE gene is the strongest genetic risk factor for Alzheimer's disease, and increasing evidence suggests that E4 carriers may respond differently to a host of dietary and metabolic-related treatments. A new appreciation is forming for the role of APOE in cerebral metabolism, and how nutritional factors may impact this role.
Considering the role dietary factors play in APOE-associated cognitive decline will help us to understand how nutritional interventions may facilitate or mitigate disease progression.
aDepartment of Physiology, University of Kentucky College of Medicine, Lexington, Kentucky
bGeriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Healthcare System
cDivision of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, Washington, USA
Correspondence to Angela J. Hanson, MD, Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine, 325 9th Ave, Box 359755, Seattle, WA 98104, USA. Tel: +1 206 897 5393; fax: +1 206 744 9976; e-mail: firstname.lastname@example.org