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Brain:阻断大脑炎症有望抑制阿尔兹海默氏症

来源:生物谷 2016-01-18 15:58

2016年1月18日讯/生物谷BIOON/近期研究表明,阻碍大脑中新型免疫细胞生产可减少阿尔茨海默病的记忆问题。南安普顿大学研究人员说他们的发现增加了证据表明大脑中炎症反应是驱动疾病的主因。

有一种药物可用来阻止生产小鼠大脑中小神经胶质细胞,并且有积极的效果。科学家说该研究结果是令人兴奋的,这可能会产生新的治疗方法。

到目前为止,大多数药物有针对性的用于治疗大脑中的淀粉样蛋白斑块,它是阿尔茨海默氏症患者独有的特征。但一项发表在《Brain》杂志上的最新研究表明,事实上,由免疫细胞积聚而成的小胶质细胞靶向大脑中的炎症可以阻止疾病的进展。

研究人员发现老年痴呆症患者的尸检大脑中小胶质细胞数量有所增加。以前的研究也表明这些细胞可能起着重要的作用。

DiegoGomez-Nicola博士说:“这些研究结果表明这个特殊的途径在阿尔茨海默氏病的发展中是非常活跃的。下一步工作是与我们的合作伙伴紧密合作,找到一个可以进行测试的安全合适的药物,观察它是否在人类中工作。”

在这项研究中,小鼠被灌注药物用来阻止CSF1R受体,该受体对它们的大脑小胶质细胞有重要意义。

药物也阻止了大脑中的神经细胞之间沟通点的消失,这通常发生在老年痴呆症患者中。MarkDallas博士说这是“一个令人激动的发现”,这就可以解释“为什么药物用于治疗阿尔茨海默氏症,但至今尚未成功”。

他补充说:“虽然基本的科学研究提供了强有力的证据,现在的问题是开发用来治疗痴呆症患者的药物,所以我们在静候临床治疗的发展。这是将实验室观察转化为可行治疗的障碍。”

DougBrown博士说,这项研究结果“令人鼓舞”。“随着人口老龄化的发展,数十多年没有新的痴呆药物的出现,现在需要找到可以减缓或阻止疾病进展的疗法。”(生物谷Bioon.com)

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Blocking the production of new immune cells in the brain could reduce memory problems seen in Alzheimer's disease, a study suggests. University of Southampton researchers said their findings added weight to evidence that inflammation in the brain is what drives the disease. A drug used to block the production of these microglia cells in the brains of mice had a positive effect. Experts said the results were exciting and could lead to new treatments. Up until now, most drugs used to treat dementia have targeted amyloid plaques in the brain which are a characteristic of people with the Alzheimer's disease. But this latest study, published in the journal Brain and funded by the Medical Research Council and Alzheimer's Research UK, suggests that in fact targeting inflammation in the brain, caused by a build-up of immune cells called microglia, could halt progression of the disease. Researchers found increased numbers of microglia in the post-mortem brains of people with Alzheimer's disease. Previous studies have also suggested that these cells could play an important role. 'Exciting discovery' Dr Diego Gomez-Nicola, lead study author from the university, said: "These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease. "The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans." In the study, mice which were given a drug to block a receptor - called CSF1R - responsible for the rise in microglia in their brains, had fewer memory and behavioural problems. The drug also prevented the loss of communication points between nerve cells in the brain which usually happens in people with Alzheimer's. Dr Mark Dallas, lecturer in cellular and molecular neuroscience at the University of Reading, said this was "an exciting discovery" which could explain "why drugs designed to treat Alzheimer's have so far been unsuccessful". He added: "While this basic science research provides strong evidence, the challenge will now be to develop medicines for people with dementia, so we await the development of clinical treatments with interest. Too often, this has been the stumbling block in turning observations in the laboratory into a workable therapy."

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