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2020作者:admin

译者声明:研究人员希望有一天能够通过药物治疗的方法治愈孤独症,其原理就是色哥窑图片区恢复自闭症患者正常的脑细胞连接

虽然研究结果令人振奋,但是距离实际临床应用还有很长的路需要走

请各位星爸星妈切勿据此文而施药!!!同时限于本人学识、专业所限,翻译难免有错漏之处,故将英文原文附后,以供大家参考

欢迎大家关注一休爸爸给他自闭症儿子开设的公众号:来自SEMBOO星

哥伦比亚大学医学中心的神经科学家最近在《神经元》杂志上发表了一篇最新的研究报告,介绍了他们的研究成果

他们通过对自闭症儿童脑组织的研究,发现这些儿童脑细胞间存在着过多突触或连接的情况,这种情况是因为大脑发育过程中出现的正常修剪过程的减缓

研究小组通过小鼠功能模型研究还发现,一种叫雷帕霉素(rapamycin)的药物能够恢复正常的突触修剪功能,并且减轻模型小鼠的类似自闭症行为

据此,他们有信心能够找到一种类似的治疗自闭症的药物,用于儿童甚至是已经确诊为自闭症的成人

自闭症者之声组织(AUTISMSPEAKER)目前正在资助与雷帕霉素相关的几项研究,同时也支持使用药物治疗研究与结节性硬化症(TSC)相关的类似孤独症的治疗

结节性硬化症(TSC)是一种非常罕见的综合症,一般情况下会同时伴有自闭症症状

事实上,哥伦比亚大学在最新的的研究中已经成功培育除了这类综合征的小鼠动物模型

自闭症者之声组织(AUTISMSPEAKER)高级副总裁和医学研究中心负责人Paul.Wang虽然并没有参与哥伦比亚大学的这项研究,但是她认为:“虽然从小鼠到人类过程中研究成果的转化还是个未知数,但是哥伦比亚大学研究的成果表明,这些药物治疗的方法有可能会对TSC患者的行为和认知产生积极影响,也可能对其他自闭症患者产生效果”

她说:“这项新的研究成果强调了在推进自闭症治疗研究方面,死后大脑捐赠的重要意义”

大脑发育过程中的重要过程——修剪在正常的大脑发育过程中,婴儿时期突触的形成非常旺盛

尤其是在在大脑皮层更为明显,因为大脑皮质是人类进行思考和处理各类信息的中枢

但到了青春期后期,大脑的修剪功能会减少大约一半的脑皮质突触

许多与自闭症有关的基因被认为会影响大脑突触的发育或功能

在检查受自闭症影响的脑组织时,研究人员发现,在儿童和青少年时期,大脑细胞的连接或突触并没有进行正常的修剪

左边的图片显示的是一个受自闭症影响的人的脑细胞,它有更丰富的突触(在每个脊椎)

右边的图片则是正常人的大脑细胞

图片来源:哥伦比亚大学医学中心 Guomei Tang/ Mark Sonders

事实上,自闭症患者有多余的突触的想法以前就有人提出过

哥伦比亚大学研究员唐国梅(音译Guomei.Tang)为了验证这个假说,进行了一系列研究

她分析了26个自闭症儿童和年轻人的大脑,其中13名儿童在2岁至9岁时死亡,13人在13岁到20岁之间

为了进行比较,她还研究了22个没有自闭症的儿童和青少年死后捐献的大脑

唐博士测量了每个大脑皮质中一小部分的突触的数量和密度

她发现,到童年后期,正常儿童(青少年)的大脑到了童年后期,大脑皮质中脑神经突触的数量和密度下降了大约一半;而与此不同的是,自闭症儿童(青少年)大脑皮质中的脑神经突触则减少了约16%

此外,她还发现了一些神经突触过多可能是因为缺乏大脑修剪所致的线索

自闭症患者的大脑细胞中存在不少损坏的细胞,缺乏正常的、医学上称之为“自噬”现象的神经突触分解途径

将该发现应用于老鼠模型利用小鼠自闭症模型,研究人员将修剪缺陷追溯到一种叫做mTOR的蛋白质

他们发现,当mTOR蛋白功能活跃时,大脑细胞会失去了大部分自我修剪功能,其结果就是大脑细胞形成了过多的突触

研究人员将一种抑制mTOR蛋白功能的药物——雷帕霉素,应用于自闭症模型小鼠身上,这种药物能够恢复正常的神经自噬和突触修剪功能

结果是,减轻了小鼠的类似自闭症行为;而且对于已经确认是自闭症行为的小鼠也产生了一定效果

据此,研究人员乐观认为,即使是已经确诊为自闭症的成年人,也有希望通过药物的方法治疗自闭症

不仅如此,通过对大量自闭症患者死后捐赠的大脑的研究发现,自闭症患者大脑中的确存在着mTOR蛋白功能过分活跃的情况

研究人员据此得出结论,虽然目前据报道有数百个基因可能与自闭症有关,但其中大多数可能是通过影响mTOR蛋白和细胞自噬这条途径从而最终导致自闭症的

英文原文 Brain Study Finds Evidence that Autism Involves TooMany Synapses A newly publishedbrain-tissue study suggests that children affected by autism have a surplus ofsynapses, or connections between brain cells. The excess is due to a slowdownin the normal pruning process that occurs during brain development, theresearchers say.The study team also found that the medication rapamycin bothrestores normal s土壤水势仪ynaptic pruning and reduces autism-like behaviors in a mousemodel of autism. They propose that someday a similar medication might be usedto treat autism after a child – or even adult – has been diagnosed.The report, by neuroscientists at ColumbiaUniversity Medical Center, appears in the journal Neuron.Autism Speaks is currently funding several studies on rapamycin. It is alsosupporting a treatment studyusing a medication with a verysimilar action for treatment of autism associated with tuberous sclerosiscomplex (TSC). This rare syndrome often, but not always, involves autism.Indeed, the laboratory mice used in the new Columbia study were developed as ananimal model of this syndrome.“There are many unknowns in translating research from mice tohumans,” comments Paul Wang, Autism Speaks senior vice president and head ofmedical research. “But the data from mice suggest that such medicines couldhave a positive effect on behavior and cognition in patients with TSC. Thefindings of this newest study might also be relevant to a subset of otherpatients with autism.” Dr. Wang was not involved in the new Columbia study.The insights from the new study also underscore the vitalimportance of post-mortem brain donations in advancing research on autismtreatments, Dr. Wang adds.During normal brain development, a burst of synapse formation occurs ininfancy. This is particularly pronounced in the cortex, which is central tothought and processing information from the senses. But by late adolescence,pruning eliminates about half of these cortical synapses.In examining brain tissue affected by autism, researchersfound that brain cell connections, or synapses, did not undergo normal pruningduring childhood and adolescence. The image on the left shows a brain cell froma person affected by autism. It has more-abundant synapses (at each spine) thanthose on a brain cell from someone unaffected by autism (right). Image credit:Guomei Tang and Mark Sonders/Columbia University Medical Center.In addition, many geneslinked to autism are known to affect the development or function of brainsynapses. Indeed, the idea that individuals with autism have excess synapseshas been proposed before.To test this hypothesis, Columbia researcher Guomei Tanganalyzed brain tissue from 26 children and young adults affected by autism.Thirteen of the children were between the ages of 2 and 9 when they died.Thirteen were between 13 to 20. For comparison, she also examined donatedpostmortem brain tissue from 22 children and teens who did not have autism.Dr. Tang measured the abundance of synapses in a small sectionof cortical tissue from each brain. She found that, by late childhood, thedensity had dropped by about half in the brain tissue unaffected by autism. Bycontrast, it was reduced by around 16 percent in the brains from individualswho had autism.She also found clues to what may have caused the lack ofpruning. The brain cells from the individuals with autism were filled withdamaged parts and deficient in signs of a normal breakdown pathway called“autophagy.” Cells use autophagy (Greek for “self-eating”) to breakdowncomponents – include synapse connections.Applying findings to mouse modelsUsing mouse models of autism, the researchers traced the pruning defect to aprotein called mTOR. When mTOR is overactive, they found, brain cells lose muchof their self-pruning ability. As a result, the brain cells show anoverabundance of synapses.The researchers restored normal autophagy and synaptic pruningin the mice by administering rapamycin – a drug that inhibits mTOR. Treatmenteliminated the mice’s autism-like behaviors. The treatment remained effectiveeven when administered to older mice that had fully developed the autism-likebehaviors.The researchers cite this as hopeful evidence that similartreatments might someday be used to treat autism after symptoms have fullyemerged. As further evidence, the researchers found large amounts of overactivemTOR in the postmortem brain tissue of the individuals with autism.Though hundreds of genes have been linked to autism, theresearcher conclude, many if not most of them may affect this mTOR/autophagypathway.色哥窑图片区