Solfrizzi Vincenzo, Colacicco Anna Maria, D'Introno Alessia, Capurso Cristiano, Parigi Angelo Del, Capurso Sabrina A, Torres Francesco, Capurso Antonio, Panza Francesco
Department of Geriatrics, Center for Aging Brain, Memory Unit, University of Bari, Bari, Italy.
J Alzheimers Dis. 2006 Nov;10(2-3):303-30. doi: 10.3233/jad-2006-102-314.
A possible role of the macronutrients and the basic elements of carbohydrates (glucose administration or depletion), proteins (amino acids such as tryptophan and tyrosine), and fat (unsaturated fatty acids) was recently proposed for age-related changes of cognitive function, and the cognitive decline of degenerative (AD) or vascular origin. The availability and utilization of glucose has been implicated in cognitive function not only as a result of nutritional and systemic metabolic conditions, but also, although speculatively, as a crucial phase of the mechanism of action of molecules used as cognitive-enhancers. Furthermore, many lines of evidence have focused on the importance of oxidative stress mechanisms and free radical damage in AD pathogenesis. In addition, epidemiological studies have recently reported an association between alcohol and the incidence of AD and predementia syndromes. Foods with large amounts of aluminium-containing additives or aluminium from drinking water may affect the risk of developing AD, aluminium more likely acting as a cofactor somewhere in the cascade of events leading to the demented brain. A role for other metals in dementia have been speculated, given the encouraging results reported from studies on peripheral zinc concentrations, zinc supplementation, serum copper, either bound with ceruloplasmin or not, and iron metabolism in AD. Nonetheless, more data are needed to support a possible role of these metals in dementing diseases. Healthy diets, antioxidant supplements, and the prevention of nutritional deficiencies or exposure to foods and water with high content of metals could be considered the first line of defence against the development and progression of cognitive decline.
最近有人提出，常量营养素以及碳水化合物（葡萄糖的给予或消耗）、蛋白质（色氨酸和酪氨酸等氨基酸）和脂肪（不饱和脂肪酸）的基本元素在认知功能的年龄相关变化以及退行性（阿尔茨海默病）或血管性起源的认知衰退中可能发挥作用。葡萄糖的可用性和利用不仅与营养和全身代谢状况有关，而且尽管具有推测性，但也与用作认知增强剂的分子作用机制的关键阶段有关，从而影响认知功能。此外，许多证据都聚焦于氧化应激机制和自由基损伤在阿尔茨海默病发病机制中的重要性。此外，流行病学研究最近报告了酒精与阿尔茨海默病和轻度认知障碍综合征发病率之间的关联。含有大量含铝添加剂的食物或饮用水中的铝可能会影响患阿尔茨海默病的风险，铝更有可能在导致痴呆大脑的一系列事件中的某个环节充当辅助因子。鉴于关于外周锌浓度、锌补充、血清铜（无论是否与铜蓝蛋白结合）以及阿尔茨海默病中铁代谢的研究报告了令人鼓舞的结果，人们推测了其他金属在痴呆症中的作用。尽管如此，仍需要更多数据来支持这些金属在痴呆疾病中可能发挥的作用。健康饮食、抗氧化剂补充剂以及预防营养缺乏或接触高金属含量的食物和水可被视为预防认知衰退发生和进展的第一道防线。
