Conclusion : [ 11c ] pib - pet detected an increased amyloid plaque load in 89 % of patients with clinically probable alzheimer disease ( ad ) 结论： pib - pet检测显示淀粉样蛋白沉积增加占临床诊断“很可能” ad的89 。
Beta ( in the form of beta - amyloid plaques ) and tau ( in the form of tau tangles ) are the physical manifestations of alzheimer ' s 贝塔（以贝塔-淀粉样斑块的形式）和陶（以陶蛋白缠结的形式）是痴呆症的物质表征。
Researchers hope to slow or een preent the deelopment of alzheimer ' s by reducing or preenting the aggregation of amyloid beta 研究者试图通过减少或阻止淀粉状蛋白的聚集来延缓甚或阻止阿耳茨海默氏病的发展。
Commonly prescribed drugs were administered in itro to brain cells deried from animal models genetically predisposed to deelop alzheimer ' s disease amyloid neuropathology 将普通处方药物用于模拟阿尔兹海默症蛋白质淀粉化神经病理的动物模型中的体外脑细胞。
Abnormally processed beta - amyloid has been identified as playing a key role in alzheimer ' s disease pathogenesis , particularly in respect to cognitie deterioration 非正常产生的-淀粉样蛋白在阿尔兹海默症的发病机理中起着关键作用，尤其在认知功能减退方面。
Amyloid plaques form when a molecule called amyloid precursor protein ( app ) is chopped up by two enzymes known as beta - secretase and gamma - secretase 当一种叫淀粉样前体蛋白（ app ）的分子被两种酶? ?分别叫作贝塔-分泌酶和伽玛-分泌酶? ?切断时就形成了淀粉样斑块。
One of the products , with the long - winded name amyloid beta - peptide 42 , has the unfortunate property that its molecules like to stick to each other 所形成的产物之一有一个冗长的名字? ?淀粉样贝塔-肽42 ，它具有一种不祥的特性，即它们分子彼此之间容易纠缠在一起。
The major factors for progressie loss of ? - cell function and mass are glucotoxicity , lipotoxicity , proinflammatory cytokines , leptin , and islet cell amyloid 导致细胞的功能与体积进行性损害的因素包括糖毒性、脂肪毒性、免疫炎性因子、瘦蛋白与胰岛细胞淀粉样变。
The major factors for progressive loss of ? - cell function and mass are glucotoxicity , lipotoxicity , proinflammatory cytokines , leptin , and islet cell amyloid 导致细胞的功能与体积进行性损害的因素包括糖毒性、脂肪毒性、免疫炎性因子、瘦蛋白与胰岛细胞淀粉样变。
To his surprise , barrio found that fddnp had a specific affinity for the neurofibrillary tangles and beta - amyloid plaques found in the brains of alzheimer ' s patients 令barrio吃惊的是，他发现fddnp对阿尔茨海默病患者脑中的神经纤维团和-淀粉样蛋白斑有特别的亲和性。
