Bibliographic
Previously, we showed that blueberry (BB) supplementation reversed the deleterious effects of aging on motor behavior and neuronal signaling in senescent rodents. We now report that BB-fed (from 4 months of age) APP 1 PS1 transgenic mice showed no deficits in Y-maze performance (at 12 months of age) with no alterations in amyloid beta burden. It appeared that the protective mechanisms are derived from BB-induced enhancement of memory-associated neuronal signaling (e.g. extracellular signal-regulated kinase) and alterations in neutral sphingomyelin-specific phospholipase C activity. Thus, our data indicate for the first time that it may be possible to overcome genetic predispositions to Alzheimer disease through diet.
Therapeutic Agent
Animal Model
Experimental Design
Number of Premature Deaths: 4 PS/APP mice died during the study – 2 in the blueberry-treated group and 2 in the control group.
Inclusion/Exclusion Criteria: 3 mice (2 PS/APP and 1 non-transgenic) were excluded from Y-maze analysis as they did not make a minimal number of choices to reliably estimate alternation frequency. These mice appeared unable/unwilling to move sufficiently to assess alternation in the task.