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【medical-news】Alzheimer's Study Raises Warning Flag
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Alzheimer's Study Raises Warning Flag
Target of drug development also critical to protection of neurons
HealthDay
Thursday, September 21, 2006
THURSDAY, Sept. 21 (HealthDay News) -- Some bad news has emerged from a study of an enzyme that is a major target in the effort to find new drugs to fight Alzheimer's disease.
Beta-secretase plays an important role in development of the protein clumps called beta-amyloid that form in Alzheimer's disease and damage mental function, so researchers are looking for compounds that might inactivate it.
But now, scientists in Germany, Belgium and the United States report in the Sept. 21 online issue of Science that beta-secretase is also involved in myelination, the formation of a protective covering for nerve cells early in life. Interfering with that activity could cause lifelong nerve damage, the researchers speculated.
The report is "a cautionary tale for scientists developing drugs today," but hardly a death blow to overall drug development for this neurodegenerative disorder, said Dr. Sam Gandy, director of the Farber Institute for Neurosciences in Philadelphia and chairman of the Alzheimer's Association medical and scientific advisory council.
The study was done in infant mice, when the protective covering forms, and "there may be no serious effects in adult life," Gandy noted.
Efforts to develop a beta-secretase inhibitor have run into problems anyway, he said. "It's very difficult to get inhibitors that are fully active and nontoxic," he explained. One practical problem is to get a pill that is small enough to be swallowed.
Furthermore, drug development efforts aren't limited to enzymes, Gandy noted. The new finding doesn't affect programs for other anti-clumping approaches or for immunotherapy, Gandy said. But, he added, "we have to be doubly cautious now that this has emerged."
Another paper in the same issue of the journal described animal experiments on the formation of the beta-amyloid clumps. The studies showed that injecting the abnormal proteins collected from Alzheimer's patients caused Alzheimer-like protein clumps in the animals.
Alzheimer's disease thus resembles brain conditions such as mad cow disease that are caused by prions, molecules which cause abnormal folding of proteins, said Lary C. Walker, a research professor in neurology at Emory University and a member of the research team.
The experiments in which abnormal beta-amyloid protein from the brains of Alzheimer's disease patients were injected into mice are part of an effort "to take our understanding of what causes the disease as far back as possible," Walker said.
The work, most of which was done at the University of Tubingen in Germany, might eventually have an application in treatment of the condition, he said. "If we can learn how the seeding process initiates these changes, we can think about different therapeutic possibilities," Walker said.
The formation of beta-amyloid protein clumps in the brain is a basic feature of Alzheimer's disease, he noted. "We have no idea now how these proteins are corrupted," Walker said. "That is what this animal model will be useful for."
HealthDay
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Alzheimer病研究发出警告
药物研究对神经元保护也非常重要
THURSDAY, Sept. 21 (HealthDay News)
在一项关于主要为了努力找到一个可以治疗Alzheimer病的酶的研究中出现一些坏消息。Beta-secretase在被称为beta-类淀粉物质（在Alzheimer病出现，并损伤认知）的蛋白块的形成过程中起重要作用，所以研究者正在寻找可以使它灭活的复合物。
但是，现在，德国、比利时和美国的科学家们在Science的网络版的Sept. 21期上报告说，beta-secretase也涉及髓鞘的形成——在生命发育早期形成神经细胞的保护层。研究者推测，干涉这个酶的活性可能会引起终生的神经损伤。
Sam Gandy博士——他是Philadelphia神经科学研究所（the Farber Institute for Neurosciences）的领导者，也是Alzheimer病相关医疗和科学建议委员会的主席——说，这个报告不仅是“对现在正在研究治疗Alzheimer病的科学家们的一个有警告意味的信息”，而且也可能是针对这种神经变性疾病的全部药物研发的致命一击（but hardly a death blow to overall drug development for this neurodegenerative disorder？）这项研究是利用乳鼠完成的，这个阶段是具有保护层作用的髓鞘的形成时期，Gandy 说“（他们觉得）这可能对成年时期没有严重影响。”他们试图研究beta-secretase抑制剂的努力工作陷入了困境，他解释说，“因为我们很难找到非常有效而又无毒的抑制剂。” 一个很实际的问题是如何做成一个很小，便于吞服的小药丸。而且，这个药物的作用不能仅局限于这些酶。Gandy说，这些新的发现并不妨碍其他的防止这些蛋白块的形成的研究或是免疫治疗，但是，他补充说，“这个问题出现以后，我们必须加倍小心。”
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作者:admin@医学,生命科学 2011-08-29 05:11
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