肿瘤生物治疗网【官方网站】

专注于生物免疫治疗技术
当前位置: 首页 > 新闻 > 健康关注 >

痴呆症或是“吃”出来的

时间:2014-03-06 11:26来源:未知 作者:donggua 点击:
近日刊登在美国《国家科学院院刊》上的一项研究指出,一种被称为晚期糖基化终末产物(AGEs)的化合物可能是淀粉样蛋白积累的一个原因,这种蛋白与阿尔兹海默氏症有关。出现在西方

  近日刊登在美国《国家科学院院刊》上的一项研究指出,一种被称为晚期糖基化终末产物(AGEs)的化合物可能是淀粉样蛋白积累的一个原因,这种蛋白与阿尔兹海默氏症有关。出现在西方饮食中的AGEs此前也被与糖尿病和神经退行性疾病联系在一起。

  与年龄有关的痴呆症和阿尔兹海默氏症目前发病率较高。无论它们的诱因还是与代谢综合征的关联目前尚不清楚。不过,以高浓度出现在血流和大脑中的AGEs已经与痴呆联系在一起,但是这种联系的机制在很大程度上仍然是未知的。

  为了找出答案,美国西奈山医学院实验糖尿病与衰老系、老年医学与保守疗法医学系的Helen Vlassara和同事追踪了摄入比例相当于西方饮食水平且有害的AGEs的小鼠的认知健康,从而判断这种化合物是否会通过抑制具有保护神经元、免疫和内分泌功能的脱乙酰基酶SIRT1而导致神经退化。

  一般而言,在患有衰老和糖尿病等大脑和代谢疾病的人体内,SIRT1呈现出不正常的低水平。研究人员报告说,与用低AGEs饮食喂养的小鼠相比,用高AGEs饮食喂养的小鼠的大脑有高水平的AGEs,而且它们的血液和大脑组织中的SIRT1水平较低。

  用高AGEs饮食喂养的小鼠出现了认知和运动功能障碍、β淀粉样蛋白沉积以及胰岛素抵抗。饮食中AGEs含量低一半的小鼠则没有表现出这些变化。

  此外,在对60岁以上的健康人群的一项临床研究中,血液中AGEs水平高的个体,其血液中的SIRT1水平也低,并且在9个月的时间里出现了认知衰退和胰岛素抵抗。作者说,通过饮食获取AGEs可能会抑制SIRT1,并最终导致痴呆症的形成。

  Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans

  Weijing Caia, Jaime Uribarrib, Li Zhua, Xue Chena, Shobha Swamya, Zhengshan Zhaoa, Fabrizio Grosjeana,c, Calogera Simonarod, George A. Kuchelc, Michal Schnaider-Beerie, Mark Woodwardf,g, Gary E. Strikera,b, and Helen Vlassaraa,b,1

  Age-associated dementia and Alzheimer’s disease (AD) are currently epidemic. Neither their cause nor connection to the metabolic syndrome (MS) is clear. Suppression of deacetylase survival factor sirtuin 1 (SIRT1), a key host defense, is a central feature of AD. Age-related MS and diabetes are also causally associated with suppressed SIRT1 partly due to oxidant glycotoxins [advanced glycation end products (AGEs)]. Changes in the modern diet include excessive nutrient-bound AGEs, such as neurotoxic methyl-glyoxal derivatives (MG). To determine whether dietary AGEs promote AD, we evaluated WT mice pair-fed three diets throughout life: low-AGE (MG?), MG-supplemented low-AGE (MG+), and regular (Reg) chow. Older MG+-fed mice, similar to old Reg controls, developed MS, increased brain amyloid-β42, deposits of AGEs, gliosis, and cognitive deficits, accompanied by suppressed SIRT1, nicotinamide phosphoribosyltransferase, AGE receptor 1, and PPARγ. These changes were not due to aging or caloric intake, as neither these changes nor the MS were present in age-matched, pair-fed MG? mice. The mouse data were enhanced by significant temporal correlations between high circulating AGEs and impaired cognition, as well as insulin sensitivity in older humans, in whom dietary and serum MG levels strongly and inversely associated with SIRT1 gene expression. The data identify a specific AGE (MG) as a modifiable risk factor for AD and MS, possibly acting via suppressed SIRT1 and other host defenses, to promote chronic oxidant stress and inflammation. Because SIRT1 deficiency in humans is both preventable and reversible by AGE reduction, a therapeutic strategy that includes AGE reduction may offer a new strategy to combat the epidemics of AD and MS.

(责任编辑:donggua)
相关文章
为什么黑巧克力对心脏有益处 痴呆症或是“吃”出来的 “太干净”易致过敏或免疫性疾 开放式办公室职员更容易生病 金-咖啡因含氮杂环类物质或可对 Nature阐析黑色素瘤迁移机制 WHO:对雾霾造成肺癌的说法持怀 常用漱口水增加心脏病和中风的
DC-CIK生物细胞免疫疗法,精确杀灭癌细胞,修复调整免疫细胞
生物治疗获冕诺贝尔医学奖桂冠
疾病症状
肝癌 肺癌 乳腺癌 胃癌 肠癌 肾癌 膀胱癌 胰腺癌 脑瘤 卵巢癌 食道癌 白血病 皮肤癌 淋巴瘤 鼻咽癌 黑色素瘤