| First Author | Beckett TL | Year | 2013 |
| Journal | Brain Res | Volume | 1505 |
| Pages | 61-7 | PubMed ID | 23415649 |
| Mgi Jnum | J:209342 | Mgi Id | MGI:5566980 |
| Doi | 10.1016/j.brainres.2013.01.046 | Citation | Beckett TL, et al. (2013) A ketogenic diet improves motor performance but does not affect beta-amyloid levels in a mouse model of Alzheimer's disease. Brain Res 1505:61-7 |
| abstractText | beta-Amyloid (Abeta), a small, fibrillogenic peptide, is known to play an important role in the pathogenesis of Alzheimer's disease (AD) in the brain. In addition, Abeta accumulates in skeletal muscle cells in individuals with sporadic inclusion body myositis (sIBM), an age-related muscle disease. Because of the socioeconomic burden associated with age-related diseases, particularly AD, there has been considerable emphasis on studying potential therapeutic strategies. The high-fat, low carbohydrate ketogenic diet has been used extensively to treat refractory childhood epilepsy and has been studied as a potential treatment for other neurological diseases, including Parkinson's disease and AD. In this study, we fed young APP/PS1 knock-in mice, which have a whole body knock-in of AD-related genes, a ketogenic diet and determined the effect on Abeta levels in the brain and skeletal muscle, as well motor performance and oxidative stress. Abeta and its precursor, the beta-C-terminal fragment of amyloid precursor protein (CTFbeta), were unchanged overall in both the brain and quadriceps after 1 month on the ketogenic diet, and there was no effect on nitrotyrosine, a product of oxidative stress. The ketogenic diet improved performance on the Rota-rod apparatus (p=0.007), however. These data indicate that the ketogenic diet may have some efficacy in the treatment of both neurologic and muscle diseases though the underlying mechanisms do not involve amelioration of Abeta pathology. |
