PDF(Pubmed)
Abstract：
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.
摘要：
杜鹃花中的黄化病的特征是叶子的叶间变黄，这通常是由缺铁引起的。这种情况通常是由于不利条件导致细胞无法正确获取铁，例如升高的pH值，而不是铁含量不足。发现萎黄病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设有相似之处。这一假设指出，铁变得螯合(例如，由淀粉样蛋白β和tau)，导致铁的功能性缺乏，破坏生化过程，导致神经变性。导致铁变得不可用的其他机制包括含铁结构没有经过适当的回收(例如，破坏的线粒体自噬和改变的铁细胞自噬)以及未能成功地将铁从一个区室转移到另一个区室(例如，由于溶酶体酸化受损）。阿尔茨海默病患者铁功能缺乏的其他原因包括血红素代谢改变或含铁蛋白及其伴侣的产生改变（例如，子单位,上游蛋白质)。对支持这一假设的证据进行了回顾。此外，讨论了阿尔茨海默病中功能性缺铁状态的机制与植物萎黄病发生的机制之间的相似之处。最后,提出了一个描述阿尔茨海默病中功能性铁缺乏的模型。
