Phenotyping of lenses from eyes of P301S tau mice

Abstract

AbstractBackgroundWe previously discovered that Aβ accumulates in the supranuclear region of the lens in the eyes of people with Alzheimer’s Disease (AD) (Goldstein et al., 2003) and Down Syndrome (DS; (Moncaster et al., 2010) and also in the Tg2576 APP swedish mutation AD mouse model (Moncaster et al., 2022). Aβ interacts with crystallin proteins in the lens to create light scattering aggregates that eventually manifest as cortical cataracts. Tau has previously been reported to be expressed in the lens of the eye (Bai et al., 2007; Zhao et al., 2013). Here we investigated whether cataracts may develop in the P301S tau model.MethodP301S mice were bred and maintained at Boston University School of Medicine. Breeder mice were purchased from Jackson Laboratories, Bar Harbor, ME. Male and Female transgenic and non‐transgenic mice (n = 5‐6 per group) were sacrificed at ages 12‐13 months. This timepoint was chosen as it is the limit of lifespan for P301S transgenic mice. Mice were perfused with phosphate buffer saline, lenses were isolated and then imaged under two different sources of light using a D70 digital Nikon camera and a custom‐adapted Zeiss stereophotomicroscope.ResultThere was no overt difference in lens phenotype between the P301S transgenic and non‐transgenic mice. No cataracts were observed in these lenses at 12‐13 months of age.ConclusionThere was no overt difference in lens phenotype between the P301S transgenic and non‐transgenic mice. Based on our current and previous results, the data suggests that Aβ may play a more significant role in lens pathology in AD than tau.