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Kathrin Kaehler, Hartwig Seitter, Adolf Sandbichler, Gerald Obermair, Nadia Stefanova, Alexandra Koschak; Morphology of the Neuroretina in Multiple System Atrophy: does the Pathology of MSA manifest in the retina?. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1884.
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© ARVO (1962-2015); The Authors (2016-present)
Due to the reported physiological and morphological abnormalities in central neurons in Parkinson's disease and Multiple System Atrophy (MSA), neurodegenerative diseases that are also associated with a variety of visual symptoms, homozygous transgenic mice overexpressing human α-SYN under the proteolipid protein (PLP)-promoter (PLP-α-SYN) were used to study morphological implications of the retina in MSA.
Immunohistochemistry was performed to investigate the expression of several relevant proteins in retinal tissue.
Distinct α-SYN signal occurred in different retinal cell layers of PLP-α-SYN, but not WT mice. This is remarkable as the PLP promotor driving the α-SYN expression in oligodendrocytes was reported to be inactive in the retina. PLP expression stopped at the optic nerve/retina junction, where we observed a colocalization with α-SYN. Notably there was one cell type distinctly stained in the central, but even more in the peripheral inner retina that was identified to be rod bipolar cells. These neurons are involved in conveying the visual information to RGCs that were also investigated by retinal wholemount stainings to test whether the overall number of RGCs is preserved. Increased glial fibrillary acidic protein (GFAP) signals in the peripheral PLP-α-SYN retina also indicated neuroinflammatory processes.
Our findings implicate an impairment of retinal neurons in the PLP-α-SYN MSA model which may also underlie visual deficits reported in MSA patients.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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