| First Author | Kashiwaya Y | Year | 2013 |
| Journal | Neurobiol Aging | Volume | 34 |
| Issue | 6 | Pages | 1530-9 |
| PubMed ID | 23276384 | Mgi Jnum | J:203371 |
| Mgi Id | MGI:5526902 | Doi | 10.1016/j.neurobiolaging.2012.11.023 |
| Citation | Kashiwaya Y, et al. (2013) A ketone ester diet exhibits anxiolytic and cognition-sparing properties, and lessens amyloid and tau pathologies in a mouse model of Alzheimer's disease. Neurobiol Aging 34(6):1530-9 |
| abstractText | Alzheimer's disease (AD) involves progressive accumulation of amyloid beta-peptide (Abeta) and neurofibrillary pathologies, and glucose hypometabolism in brain regions critical for memory. The 3xTgAD mouse model was used to test the hypothesis that a ketone ester-based diet can ameliorate AD pathogenesis. Beginning at a presymptomatic age, 2 groups of male 3xTgAD mice were fed a diet containing a physiological enantiomeric precursor of ketone bodies (KET) or an isocaloric carbohydrate diet. The results of behavioral tests performed at 4 and 7 months after diet initiation revealed that KET-fed mice exhibited significantly less anxiety in 2 different tests. 3xTgAD mice on the KET diet also exhibited significant, albeit relatively subtle, improvements in performance on learning and memory tests. Immunohistochemical analyses revealed that KET-fed mice exhibited decreased Abeta deposition in the subiculum, CA1 and CA3 regions of the hippocampus, and the amygdala. KET-fed mice exhibited reduced levels of hyperphosphorylated tau deposition in the same regions of the hippocampus, amygdala, and cortex. Thus, a novel ketone ester can ameliorate proteopathic and behavioral deficits in a mouse AD model. |
