| First Author | Gratuze M | Year | 2016 |
| Journal | Neurobiol Aging | Volume | 47 |
| Pages | 71-73 | PubMed ID | 27565300 |
| Mgi Jnum | J:239559 | Mgi Id | MGI:5829152 |
| Doi | 10.1016/j.neurobiolaging.2016.07.016 | Citation | Gratuze M, et al. (2016) High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology. Neurobiol Aging 47:71-73 |
| abstractText | Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice. |
