PDF(Pubmed)
Abstract：
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 R2 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.
摘要：
视网膜高光谱成像（HSI）是一种非侵入性的体内方法，已在阿尔茨海默氏病中显示出希望。帕金森病是另一种神经退行性疾病，其中脑病理学如α-突触核蛋白和铁的过度积累与视网膜有关。然而,尚不清楚HSI在帕金森病的体内模型中是否发生改变，它是否不同于健康的衰老，以及推动这些变化的机制。为了解决这个问题，我们在两个不同年龄的帕金森病小鼠模型中进行了HSI；α-突触核蛋白过度积累模型（hA53T转基因株系M83，A53T）和铁沉积模型（Tau敲除，TauKO).与野生型同窝相比，A53T和TauKO小鼠在短波长〜450至600nm处的反射率均增加。相比之下,三个背景菌株的健康衰老表现出相反的效果，在短波长光谱中反射率降低。我们还证明了帕金森的高光谱特征与阿尔茨海默病模型相似，5xFAD小鼠。当相对于年龄作图时，HSI的多变量分析是有意义的。此外，当α-突触核蛋白，添加铁或视网膜神经纤维层厚度作为辅因子，这改善了某些组中相关性的R2值。这项研究证明了帕金森病的体内高光谱特征，这在两个小鼠模型中是一致的，并且与健康衰老不同。还有一个建议，包括α-突触核蛋白和铁的视网膜沉积在内的因素可能在晚期衰老中驱动帕金森氏病的高光谱轮廓和视网膜神经纤维层厚度中起作用。这些发现表明，HSI可能是帕金森病的一个有前途的翻译工具。
