| First Author | Joly S | Year | 2017 |
| Journal | Neurobiol Aging | Volume | 53 |
| Pages | 181-191 | PubMed ID | 28262325 |
| Mgi Jnum | J:243377 | Mgi Id | MGI:5908317 |
| Doi | 10.1016/j.neurobiolaging.2017.02.004 | Citation | Joly S, et al. (2017) Nonamyloidogenic processing of amyloid beta precursor protein is associated with retinal function improvement in aging male APPswe/PS1DeltaE9 mice. Neurobiol Aging 53:181-191 |
| abstractText | Vision declines during normal aging and in Alzheimer's disease (AD). Although the toxic role of amyloid beta (Abeta) has been established in AD pathogenesis, its influence on the aging retina is unclear. Using APPswe/PS1DeltaE9 transgenic (TG) mice, a classical AD model, the retinal cell function and survival was assessed by electroretinogram (ERG) recordings and immunofluorescent stainings. Strikingly, photopic ERG measurements revealed that the retinal response mediated by cones was preserved in aging TG mice relative to WT controls. In contrast to the cortex, the expression of mutated APPswe and PS1DeltaE9 did not allow to detect Abeta or amyloid plaques in 13-month-old male TG retinae. In addition, the CTFbeta/CTFalpha ratio was significantly lower in retinal samples than that in cortical extracts, suggesting that the nonamyloidogenic pathway may endogenously limit Abeta formation in the retina of male mice. Collectively, our data suggest that retinal-specific processing of amyloid may confer protection against AD and selectively preserve cone-dependent vision during aging. |
