Age-related macular degeneration (AMD) is a common retinal disorder, which became more and more prevalent in the last decades. AMD is now the most prevalent cause of blindness in the western world. The disorder is classified into two phenotypes named dry and wet AMD. This is based on the recruitment of novel blood vessels and inflammatory exudates in wet AMD. In both phenotypes, the pathological hallmark is the presence of proteinaceous aggregates called drusen, which mostly accumulate between the choroid and the retinal pigment. Drusen in dry AMD represent the evident pathological finding although they are present, though less defined, in wet AMD. In AMD drusen are supposed to be a pathogenic trigger of the disorder. In fact, drusen may mechanically alter retinal function. A novel hypothesis exists, suggesting that a metabolic defect (systemic or focal within the retinal pigment epithelium) may be the real determinant of visual impairment, while causing the concomitant accumulation of proteinaceous debris and lipids forming the drusen. Here we face such an issue by analyzing the retinal anatomy to correlate visual impairment with the occurrence of drusen number, size and the extent of a drusenoid area in the foveal region. A comparison is made with wet AMD where new vessels and retinal exudates prevail. The study is carried out in 120 patients affected by dry or wet AMD and 21 patients where paradoxical findings are described. The main question consists in inferring whether the occurrence of visual impairment is due, in fact, to a drusen-dependent mechanical damage or drusen just occurs as an independent consequence of an upstream metabolic alteration, which concomitantly impairs the visual process. The present data indicate that, despite a significant difference in visual function between mild and severe AMD patients in the amount of drusen exists, a strong correlation between drusen and visual impairment does not occur. This suggests that drusen and visual deterioration develop as a consequence of similar upstream biochemical alterations but it is likely that drusen do not produce visual deterioration. This is strengthened here by extreme clinical conditions, where visual impairment is severe with a slight alteration in the planar pattern of the retina or, vice versa an extended drusenoid area occurs concomitantly with fair visual acuity, contrast sensitivity and lack of metamorphopsia. A biochemical analysis of key areas in the function of specific domains in the pigment epithelium as described in the accompanying manuscript should help to better disclose the real morpho-functional deficit, which takes place in AMD.

中文翻译：

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受年龄相关性黄斑变性影响的患者玻璃膜疣的测量及其与视觉症状的相关性。

年龄相关性黄斑变性（AMD）是一种常见的视网膜疾病，在最近几十年中变得越来越普遍。AMD现在是西方世界最普遍的失明原因。该疾病分为两种表型，分别称为干性和湿性AMD。这是基于湿性AMD中新血管和炎性渗出物的募集。在这两种表型中，病理学特征是存在被称为玻璃疣的蛋白质聚集体，其主要聚集在脉络膜和视网膜色素之间。干燥AMD中的玻璃疣表现出明显的病理学发现，尽管存在于湿性AMD中，尽管定义较不明确。在AMD中，玻璃疣被认为是该疾病的致病性诱因。实际上，玻璃疣可能会机械改变视网膜功能。存在一个新的假设 提示代谢缺陷（视网膜色素上皮内的系统性或局灶性）可能是视力障碍的真正决定因素，同时引起蛋白质碎片和脂质的积累，从而形成玻璃疣。在这里，我们通过分析视网膜解剖结构以使视力障碍与小凹区域的小疣数目，大小和小疣区域的程度相关联，从而面临这样的问题。与湿性AMD进行比较，其中以新血管和视网膜渗出物为主。这项研究在120名受干或湿性AMD感染的患者和21名描述了矛盾发现的患者中进行。主要问题在于推断视力障碍的发生是否应归因于事实上，依赖于玻璃疣的机械损伤或玻璃疣只是作为上游代谢改变的独立结果而发生的，其同时损害了视觉过程。目前的数据表明，尽管轻度和重度AMD患者之间在视神经功能方面存在明显的玻璃膜疣量差异，但玻璃膜疣与视力障碍之间并没有发生强烈的相关性。这表明由于相似的上游生化改变而导致玻璃疣和视觉恶化，但是玻璃疣可能不会产生视觉恶化。这在极端的临床条件下得到了加强，在这种情况下，视力障碍严重，视网膜的平面图案稍有改变，反之亦然，扩大的类杜鹃样区域会出现，并伴有明显的视力，对比敏感度和缺乏变形。如所附手稿中所述，对色素上皮中特定域功能关键区域的生化分析应有助于更好地揭示在AMD中发生的真正的形态功能缺陷。