Alzheimer's Disease (AD) is a devastating neurodegenerative disorder of the brain, clinically characterised by cognitive deficits that gradually worsen over time. There is, at present, no established cure, or disease-modifying treatments for AD. As life expectancy increases globally, the number of individuals suffering from the disease is projected to increase substantially. Cumulative evidence indicates that AD neuropathological process is initiated several years, if not decades, before clinical signs are evident in patients, and diagnosis made. While several imaging, cognitive, CSF and blood-based biomarkers have been proposed for the early detection of AD; their sensitivity and specificity in the symptomatic stages is highly variable and it is difficult to justify their use in even earlier, pre-clinical stages of the disease. Research has identified potentially measurable functional, structural, metabolic and vascular changes in the retina during early stages of AD. Retina offers a distinctively accessible insight into brain pathology and current and developing ophthalmic technologies have provided us with the possibility of detecting and characterising subtle, disease-related changes. Recent human and animal model studies have further provided mechanistic insights into the biochemical pathways that are altered in the retina in disease, including amyloid and tau deposition. This information coupled with advances in molecular imaging has allowed attempts to monitor biochemical changes and protein aggregation pathology in the retina in AD. This review summarises the existing knowledge that informs our understanding of the impact of AD on the retina and highlights some of the gaps that need to be addressed. Future research will integrate molecular imaging innovation with functional and structural changes to enhance our knowledge of the AD pathophysiological mechanisms and establish the utility of monitoring retinal changes as a potential biomarker for AD.

阿尔茨海默病 (AD) 是一种破坏性的大脑神经退行性疾病，其临床特征是认知缺陷，随着时间的推移逐渐恶化。目前，对于 AD 还没有确定的治愈方法或改善疾病的治疗方法。随着全球预期寿命的增加，预计患有该疾病的人数将大幅增加。累积证据表明，AD 神经病理学过程在患者出现明显的临床症状和做出诊断之前的几年甚至几十年就开始了。虽然已经提出了几种基于成像、认知、CSF 和血液的生物标志物用于 AD 的早期检测；它们在症状阶段的敏感性和特异性变化很大，很难证明它们在疾病的更早、临床前阶段的使用是合理的。研究已经确定了 AD 早期阶段视网膜中潜在的可测量的功能、结构、代谢和血管变化。视网膜提供了对大脑病理学的独特见解，当前和正在发展的眼科技术为我们提供了检测和表征与疾病相关的细微变化的可能性。最近的人类和动物模型研究进一步提供了对疾病中视网膜发生改变的生化途径的机械见解，包括淀粉样蛋白和 tau 沉积。这些信息与分子成像的进步相结合，可以尝试监测 AD 视网膜中的生化变化和蛋白质聚集病理。本综述总结了现有知识，这些知识有助于我们理解 AD 对视网膜的影响，并强调了一些需要解决的差距。未来的研究将分子成像创新与功能和结构变化相结合，以增强我们对 AD 病理生理机制的了解，并建立监测视网膜变化作为 AD 潜在生物标志物的实用性。