Department of Optometry and Vision Sciences, University of Melbourne, Parkville, VIC, 3010, Australia.
Florey Institute of Neuroscience and Mental Health, Parkville, VIC, 3010, Australia.
Sci Rep. 2024 Jul 12;14(1):16089. doi: 10.1038/s41598-024-66284-7.
Retinal hyperspectral imaging (HSI) is a non-invasive in vivo approach that has shown promise in Alzheimer's disease. Parkinson's disease is another neurodegenerative disease where brain pathobiology such as alpha-synuclein and iron overaccumulation have been implicated in the retina. However, it remains unknown whether HSI is altered in in vivo models of Parkinson's disease, whether it differs from healthy aging, and the mechanisms which drive these changes. To address this, we conducted HSI in two mouse models of Parkinson's disease across different ages; an alpha-synuclein overaccumulation model (hA53T transgenic line M83, A53T) and an iron deposition model (Tau knock out, TauKO). In comparison to wild-type littermates the A53T and TauKO mice both demonstrated increased reflectivity at short wavelengths ~ 450 to 600 nm. In contrast, healthy aging in three background strains exhibited the opposite effect, a decreased reflectance in the short wavelength spectrum. We also demonstrate that the Parkinson's hyperspectral signature is similar to that from an Alzheimer's disease model, 5xFAD mice. Multivariate analyses of HSI were significant when plotted against age. Moreover, when alpha-synuclein, iron or retinal nerve fibre layer thickness were added as a cofactor this improved the R values of the correlations in certain groups. This study demonstrates an in vivo hyperspectral signature in Parkinson's disease that is consistent in two mouse models and is distinct from healthy aging. There is also a suggestion that factors including retinal deposition of alpha-synuclein and iron may play a role in driving the Parkinson's disease hyperspectral profile and retinal nerve fibre layer thickness in advanced aging. These findings suggest that HSI may be a promising translation tool in Parkinson's disease.
视网膜高光谱成像(HSI)是一种非侵入性的体内方法,在阿尔茨海默病中显示出了前景。帕金森病是另一种神经退行性疾病,其中脑病理生物学,如α-突触核蛋白和铁过度积累,与视网膜有关。然而,目前尚不清楚 HSI 是否在帕金森病的体内模型中发生改变,它是否与健康衰老不同,以及驱动这些变化的机制是什么。为了解决这个问题,我们在两种不同年龄的帕金森病小鼠模型中进行了 HSI 研究;一种是α-突触核蛋白过度积累模型(hA53T 转基因系 M83,A53T)和一种是铁沉积模型(Tau 敲除,TauKO)。与野生型同窝仔相比,A53T 和 TauKO 小鼠在短波长(~450 至 600nm)下的反射率都增加了。相比之下,三种背景品系的健康衰老表现出相反的效果,即短波长光谱下的反射率降低。我们还证明,帕金森病的高光谱特征与阿尔茨海默病模型,5xFAD 小鼠相似。当以年龄为横坐标进行 HSI 的多元分析时,结果具有统计学意义。此外,当将α-突触核蛋白、铁或视网膜神经纤维层厚度作为协变量添加时,这会提高某些组中相关性的 R 值。这项研究表明,在两种小鼠模型中,帕金森病存在一种体内高光谱特征,与健康衰老不同。还有一种说法是,包括视网膜α-突触核蛋白和铁沉积在内的因素可能在驱动帕金森病高光谱特征和衰老后期的视网膜神经纤维层厚度方面发挥作用。这些发现表明,HSI 可能是帕金森病有前途的转化工具。