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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #367771

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies

Location: Virus and Prion Research

Title: Retina as a model to study in vivo transmission of alpha-synuclein in the A53T mouse model of Parkinson’s disease

Author
item MAMMADOVA, NAJIBA - ORISE FELLOW
item BARON, THIERRY - FRENCH AGENCY FOR FOOD, ENVIRONMENTAL AND OCCUPATIONAL HEALTH & SAFETY (ANSES)
item VERCHERE, JEREMY - FRENCH AGENCY FOR FOOD, ENVIRONMENTAL AND OCCUPATIONAL HEALTH & SAFETY (ANSES)
item Greenlee, Justin
item WEST GREENLEE, M - IOWA STATE UNIVERSITY

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 3/10/2020
Publication Date: 2/20/2021
Citation: Mammadova, N., Baron, T., Verchere, J., Greenlee, J.J., West Greenlee, M.H. 2021. Retina as a model to study in vivo transmission of alpha-synuclein in the A53T mouse model of Parkinson’s disease. In: Singh S.R., Hoffman R.M., Singh A. (eds) Mouse Genetics. Methods in Molecular Biology. New York, NY: Humana. p.75-85. https://doi.org/10.1007/978-1-0716-1008-4_5.
DOI: https://doi.org/10.1007/978-1-0716-1008-4_5

Interpretive Summary:

Technical Abstract: Parkinson's disease is a neurodegenerative disorder characterized by accumulation of misfolded alpha-synuclein within the central nervous system (CNS). Retinal manifestations have been widely described as a preclinical, however we have a limited understanding of the retinal pathology associated with Parkinson’s disease. The strong similarities between the retina and the brain and the accessibility of the retina has potentiated studies to investigate retinal pathology in an effort to identify biomarkers for early detection, as well as for monitoring the progression of disease and efficacy of therapies as they become available. Here, we discuss a study conducted using a transgenic mouse model of Parkinson’s disease (TgM83, expressing human alpha-synuclein containing the familial PD-associated A53T mutation) to demonstrate the effect of the A53T alpha-synuclein mutation on the retina. Additionally, we show that “seeding” with brain homogenates from clinically ill TgM83 mice accelerates the accumulation of retinal alpha-synuclein. The work described in this chapter provides insight into retinal changes associated with Parkinson's disease, and identifies retinal indicators of Parkinson’s disease pathogenesis that could serve as potential biomarkers for early detection.