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Juliet A Moncaster, Mark W Wojnarowicz, Olga Minaeva, Srikant Sarangi, Zoe Brasher, Rebecca Zeng, Lee E Goldstein; Aβ-potentiated and Aβ-independent age-related changes in the lens of wild-type and Alzheimer’s Disease mice. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5311. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Crystallins comprise ~90% of lens protein in mature lens fiber cells and undergo various post-translational modifications during aging that disrupt the normal functioning of the proteins, facilitating aggregation, insolubilization and light scattering. Crystallins have been shown to interact with Aβ in particular in Alzheimer’s disease. Here, we expand on previous work by us and others and investigated the aging effect of crystallins in an Aβ-independent and Aβ-potentiated environment and the effect on light scattering in lenses from aged (27 months) wild-type and Alzheimer’s disease transgenic mice (Tg2576).
Mice were bred, maintained and genotyped at Boston University. Mice were sacrificed at 27 months of age, 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.
Wild-type aged mice demonstrated light scattering in two distinct concentric layers (cortical and outer nuclear) in the lens compared to young mice. Furthermore, Tg2576 aged mice showed increased scattering in the cortical layer compared to wild-type aged mice.
Two distinct light scattering layers of the lens are affected during aging involving Aβ-potentiated mechanisms in Tg2576 mice and Aβ-independent mechanisms in wild-type mice.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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