| First Author | Manocha GD | Year | 2019 |
| Journal | Neurobiol Aging | Volume | 81 |
| Pages | 166-176 | PubMed ID | 31284126 |
| Mgi Jnum | J:281639 | Mgi Id | MGI:6378391 |
| Doi | 10.1016/j.neurobiolaging.2019.05.025 | Citation | Manocha GD, et al. (2019) Temporal progression of Alzheimer's disease in brains and intestines of transgenic mice. Neurobiol Aging 81:166-176 |
| abstractText | The amyloid beta (Abeta) peptide is associated with the neurodegenerative and inflammatory changes in brains affected by Alzheimer's disease (AD). We hypothesized that the enteric nervous system also produces Abeta in an intestinal component of disease. To test this idea, we compared C57BL/6 wild-type (WT) male and female mice to two models of Alzheimer's disease, amyloid precursor protein (APP)/presenilin 1 (PS1) mice and amyloid precursor protein NL-G-F (App(NL-G-F)) mice, at 3, 6, and 12 months of age. Brain Abeta plaque deposition in App(NL-G-F) mice preceded that in the APP/PS1 mice, observable by 3 months. Three-month-old female App(NL-G-F) mice had decreased intestinal motility compared with WT and APP/PS1 mice. However, 3-month-old female APP/PS1 mice demonstrated increased intestinal permeability compared with WT and App(NL-G-F) mice. Both sexes of APP/PS1 and App(NL-G-F) mice demonstrated increased colon lipocalin 2 mRNA and insoluble Abeta 1-42 levels at 3 months. These data demonstrate an unrecognized enteric aspect of disease in 2 different mouse models correlating with the earliest brain changes. |
