Retinal Alpha-Synuclein Accumulation Correlates With Retinal Dysfunction and Structural Thinning In The A53T Mouse Model of Parkinson’S Disease

Authors

Katie K N Tran
Vickie H Y Wong
Anh Hoang
David I Finkelstein
Bang V Bui
Christine T O Nguyen

Language

English

Publication Date

1-1-2023

Journal

Frontiers in Neuroscience

DOI

10.3389/fnins.2023.1146979

PMID

37214398

PMCID

PMC10196133

PubMedCentral® Posted Date

May 2023

PubMedCentral® Full Text Version

Post-print

Abstract

Abnormal alpha-synuclein (α-SYN) protein deposition has long been recognized as one of the pathological hallmarks of Parkinson's disease's (PD). This study considers the potential utility of PD retinal biomarkers by investigating retinal changes in a well characterized PD model of α-SYN overexpression and how these correspond to the presence of retinal α-SYN. Transgenic A53T homozygous (HOM) mice overexpressing human α-SYN and wildtype (WT) control littermates were assessed at 4, 6, and 14  months of age (male and female,

Keywords

A53T, alpha-synuclein, Parkinson’s disease, retina, electroretinography, optical coherence tomography

Published Open-Access

yes

Recommended Citation

Tran, Katie K N; Wong, Vickie H Y; Hoang, Anh; et al., "Retinal Alpha-Synuclein Accumulation Correlates With Retinal Dysfunction and Structural Thinning In The A53T Mouse Model of Parkinson’S Disease" (2023). Faculty, Staff and Student Publications. 2340.
https://digitalcommons.library.tmc.edu/uthmed_docs/2340