Chlorosis in azaleas is characterized by an interveinal yellowing of leaves that is typically caused by a deficiency of iron. This condition is usually due to the inability of cells to properly acquire iron as a consequence of unfavorable conditions, such as an elevated pH, rather than insufficient iron levels. The causes and effects of chlorosis were found to have similarities with those pertaining to a recently presented hypothesis that describes a pathogenic process in Alzheimer disease. This hypothesis states that iron becomes sequestered (e.g., by amyloid β and tau), causing a functional deficiency of iron that disrupts biochemical processes leading to neurodegeneration. Additional mechanisms that contribute to iron becoming unavailable include iron-containing structures not undergoing proper recycling (e.g., disrupted mitophagy and altered ferritinophagy) and failure to successfully translocate iron from one compartment to another (e.g., due to impaired lysosomal acidification). Other contributors to a functional deficiency of iron in patients with Alzheimer disease include altered metabolism of heme or altered production of iron-containing proteins and their partners (e.g., subunits, upstream proteins). A review of the evidence supporting this hypothesis is presented. Also, parallels between the mechanisms underlying a functional iron-deficient state in Alzheimer disease and those occurring for chlorosis in plants are discussed. Finally, a model describing the generation of a functional iron deficiency in Alzheimer disease is put forward.

中文翻译：

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阿尔茨海默病的杜鹃花假说：功能性缺铁促进神经退行性变。

杜鹃花失绿的特点是叶子脉间变黄，这通常是由缺铁引起的。这种情况通常是由于不利条件（例如 pH 升高）导致细胞无法正确获取铁，而不是铁水平不足。研究发现，萎黄症的原因和影响与最近提出的描述阿尔茨海默病致病过程的假说有相似之处。该假说指出，铁被隔离（例如，通过β淀粉样蛋白和tau蛋白），导致铁的功能性缺乏，从而破坏生化过程，导致神经退行性变。导致铁无法利用的其他机制包括含铁结构未进行适当的回收（例如，线粒体自噬破坏和铁蛋白自噬改变）以及未能成功地将铁从一个区室转移到另一区室（例如，由于溶酶体酸化受损）。阿尔茨海默病患者铁功能性缺乏的其他因素包括血红素代谢改变或含铁蛋白质及其伴侣（例如亚基、上游蛋白质）的产生改变。对支持这一假设的证据进行了回顾。此外，还讨论了阿尔茨海默病功能性缺铁状态的机制与植物失绿症发生机制之间的相似之处。最后，提出了一个描述阿尔茨海默病功能性缺铁产生的模型。