| First Author | Tran KKN | Year | 2023 |
| Journal | Front Neurosci | Volume | 17 |
| Pages | 1146979 | PubMed ID | 37214398 |
| Mgi Jnum | J:339114 | Mgi Id | MGI:7485042 |
| Doi | 10.3389/fnins.2023.1146979 | Citation | Tran KKN, et al. (2023) Retinal alpha-synuclein accumulation correlates with retinal dysfunction and structural thinning in the A53T mouse model of Parkinson's disease. Front Neurosci 17:1146979 |
| abstractText | Abnormal alpha-synuclein (alpha-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 alpha-SYN overexpression and how these correspond to the presence of retinal alpha-SYN. Transgenic A53T homozygous (HOM) mice overexpressing human alpha-SYN and wildtype (WT) control littermates were assessed at 4, 6, and 14 months of age (male and female, n = 15-29 per group). In vivo retinal function (electroretinography, ERG) and structure (optical coherence tomography, OCT) were recorded, and retinal immunohistochemistry and western blot assays were performed to examine retinal alpha-SYN and tyrosine hydroxylase. Compared to WT controls, A53T mice exhibited reduced light-adapted (cone photoreceptor and bipolar cell amplitude, p < 0.0001) ERG responses and outer retinal thinning (outer plexiform layer, outer nuclear layer, p < 0.0001) which correlated with elevated levels of alpha-SYN. These retinal signatures provide a high throughput means to study alpha-SYN induced neurodegeneration and may be useful in vivo endpoints for PD drug discovery. |
