Squitti Rosanna, Siotto Mariacristina, Polimanti Renato
Fatebenefratelli Foundation for Health Research and Education, AFaR Division, "San Giovanni Calibita" Fatebenefratelli Hospital, Rome, Italy; Laboratorio di Neurodegenerazione, IRCCS San Raffaele Pisana, Rome, Italy.
Don Carlo Gnocchi Foundation ONLUS, Milan, Italy.
Neurobiol Aging. 2014 Sep;35 Suppl 2:S40-50. doi: 10.1016/j.neurobiolaging.2014.02.031. Epub 2014 May 15.
Copper is an essential element, and either a copper deficiency or excess can be life threatening. Recent studies have indicated that alteration of copper metabolism is one of the pathogenetic mechanisms of Alzheimer's disease (AD). In light of these findings, many researchers have proposed preventive strategies to reduce AD risk. Because the general population comes in contact with copper mainly through dietary intake, that is, food 75% and drinking water 25%, a low-copper diet can reduce the risk of AD in individuals with an altered copper metabolism. We suggest that a diet-gene interplay is at the basis of the "copper phenotype" of sporadic AD. Herein, we describe the pathways regulating copper homeostasis, the adverse sequelae related to its derangements, the pathogenic mechanism of the AD copper phenotype, indications for a low-copper diet, and future perspectives to improve this preventive strategy.
铜是一种必需元素，铜缺乏或过量都可能危及生命。最近的研究表明，铜代谢改变是阿尔茨海默病（AD）的发病机制之一。鉴于这些发现，许多研究人员提出了降低AD风险的预防策略。由于普通人群主要通过饮食摄入接触铜，即食物占75%，饮用水占25%，低铜饮食可以降低铜代谢改变个体患AD的风险。我们认为饮食-基因相互作用是散发性AD“铜表型”的基础。在此，我们描述了调节铜稳态的途径、与其紊乱相关的不良后果、AD铜表型的致病机制、低铜饮食的指征以及改善这一预防策略的未来展望。
