Galaburda Albert M
Harvard Medical School, Division of Behavioral Neurology and Memory Disorders, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Ann Dyslexia. 2005 Dec;55(2):151-65. doi: 10.1007/s11881-005-0009-4.
For 25 years now, there has been a serious attempt to get at the fundamental cause(s) of dyslexia in our laboratory. A great deal of research has been carried out on the psychological and brain underpinnings of the linguistic dysfunctions seen in dyslexia, but attempts to get at its cause have been limited. Initially, observations were made on the brains of persons with dyslexia who had died and their brains donated for research. These observations were modeled in animal models in order to better understand the full extent of anatomical and developmental brain characteristics. More recently, models have begun to employ genetic manipulations in order to close the gap between genes, brain, and behavior. In this article based on a lecture given in memory of Dr. Norman Geschwind to the International Dyslexia Association assembly in Philadelphia in 2004, I outline the history of the research leading up to the most recent findings. These findings consist of experiments using methods that interfere with the function of DNA, using as constructs genes that have been implicated in dyslexia, which cause developmental problems of neuronal migration in rats, secondary brain changes in response to the migration problems, and abnormal processing of sounds.
25年来，我们实验室一直在认真尝试探寻诵读困难的根本原因。针对诵读困难中出现的语言功能障碍的心理和大脑基础，已经开展了大量研究，但探寻其病因的尝试却很有限。最初，我们对已故的诵读困难患者的大脑进行了观察，这些大脑是捐赠用于研究的。这些观察结果在动物模型中进行了模拟，以便更好地了解大脑解剖结构和发育特征的全貌。最近，模型开始采用基因操作，以缩小基因、大脑和行为之间的差距。在这篇基于2004年在费城国际诵读困难协会大会上为纪念诺曼·杰施温德博士而发表的演讲的文章中，我概述了导致最新研究结果的研究历史。这些研究结果包括使用干扰DNA功能的方法进行的实验，所使用的构建基因与诵读困难有关，这些基因会导致大鼠神经元迁移的发育问题、大脑对迁移问题的继发性变化以及声音的异常处理。
