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科学家发现可能导致阿尔茨海默病的新蛋白质_我的网站

A |     阿尔茨海默病（AD）是一种使人衰弱的渐进性疾病，开始时是轻微的记忆丧失，慢慢地破坏了认知功能和记忆。

B |     SAVANNAH, Ga. -- A Georgia man was left reeling after receiving a $1.4 million speeding ticket, but city officials say the figure was just a placeholder, not the actual fine.Connor Cato tells WSAV-TV in Savannah that he received the citation after getting pulled over in September for driving 90 mph (145 kph) in a 55 mph (89 kph) zone.He called the court thinking the figure was a typo but says he was told he either had to pay it or appear in court in December.Savannah officials say anyone caught driving more than 35 mph (56 kph) above the speed limit has to appear in court, where a judge will determine the actual fine.The figure Cato received reflected a “placeholder” that was automatically generated by e-citation software used by the local Recorder's Court, said Joshua Peacock, a spokesman for Savannah's city government. The actual fine cannot exceed $1,000 in addition to state-mandated costs.“We do not issue that placeholder as a threat to scare anybody into court, even if this person heard differently from somebody in our organization,” Peacock told The Associated Press. He added that the court “is currently working on adjusting the placeholder language to avoid any confusion.”。它目前没有治愈方法，预计到2050年将影响全球1亿多人。在美国，根据国家老龄化研究所的数据，AD是老年人痴呆的主要原因，也是第七大最常见的死亡原因。正在进行的阿尔茨海默氏症研究集中在两个关键的神经毒性蛋白上：淀粉样β（Aβ）和tau。尽管这些蛋白质已被证明与AD有关，但Aβ和tau的水平并不能持续解释或与一些疾病患者的认知能力下降的严重程度相关。作为麻省总医院布里格姆医疗系统的创始成员之一，布里格姆妇女医院的研究人员着手确定其他可能直接参与AD基本方面的蛋白质，如突触损失和神经变性。他们将实验室的神经元暴露在大约40人的大脑提取物中，这些人要么患有AD，要么在Aβ和tau水平较高的情况下受到保护，要么在大脑中很少或没有Aβ和tau时受到保护。科学家们发现并验证了神经节苷脂GM2激活剂（GM2A）是一种能够减少神经元发射并诱发神经元完整性丧失的蛋白质。这些蛋白质的特征可能有助于AD的病因、疾病的进展，或两者都有。高级作者、神经学系的Tracy Young-Pearse博士说："我们的数据有助于确定一种可能与阿尔茨海默病的发病机制有关的新的和潜在的重要蛋白质。有趣的是，GM2A以前被认为是一种与Tay-Sachs病非常相似的溶酶体储存障碍的致病因素，Tay-Sachs病是另一种像AD一样破坏神经元的疾病。

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