ARCHITECTURE AND CONNECTIVITY OF MINOR CORTICAL MALFORMATIONS

轻微皮质畸形的结构和连接性

• 批准号: 5212609
• 负责人: ALBERT M GALABURDA
• 金额: --
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/5212609
• 关键词: autoimmune disorder; biological models; biomarker; brain disorders; brain imaging /visualization /scanning; brain injury; cell sorting; cell type; central neural pathway /tract; cerebral cortex; developmental neurobiology; experimental brain lesion; fluorescence microscopy; genetic strain; histopathology; immunocytochemistry; immunodeficiency; laboratory mouse; morphology; neuroanatomy; neurons; psychoneuroimmunology; reading disorder; stainings

Molecular layer ectopias and microgyria have been seen in the brains of dyslexic subjects. Immune-defective mice spontaneously develop molecular layer ectopias, and we have successfully induced microgyria in rats and mice. Both humans and animals with these minor cortical malformations exhibit behavioral abnormalities. Preliminary findings have shown that both the spontaneous (SMM) and the induced (IMM) malformations are associated with a more widespread cortical disorganization than is readily apparent. We suspect that it is this architectonic and connectional disorganization that is responsible for the behavioral abnormalities. In the present research, we propose to show the extent of cellular changes associated with SMM and IMM and the connectional changes associated with IMM. We will examine SMM from the breeding Core as well as from the Embryo Transfer research, the latter to look for effects of uterine manipulations on the final structure of the SMM. We will examine IMM that have been produced by varying timing and severity of injury at the onset, to assess these factors with respect to the final structure of the IMM. Minor cortical malformations in humans are receiving increasing attention, but their etiology and significance are unknown. We have seen them to be related to at least one form of learning disability -- developmental dyslexia. We expect that this research will shed light on the nature of the cortical malformations and their possible consequences on behavior.

在大脑中已经看到了分子层的异位症和小毛病 阅读障碍受试者。 免疫缺陷的小鼠自发发展分子 层的ectopias，我们已经成功诱导了大鼠的小胶质细胞质 老鼠。 人类和动物都有这些较小的皮质畸形 表现出行为异常。 初步发现表明 自发（SMM）和诱导的（IMM）畸形都是 与更广泛的皮质混乱相关，而不是容易 显而易见。 我们怀疑是这种建筑和连接 导致行为异常的混乱。 在 本研究，我们建议显示细胞变化的程度 与SMM和IMM相关联以及与之相关的连接变化 imm。 我们将检查来自育种核心以及胚胎的SMM 转移研究，后者寻找子宫操作的影响 关于SMM的最终结构。 我们将检查已经 通过在发病时发生的时间和严重程度变化而产生的，以评估 这些因IMM的最终结构的因素。 次要的 人类的皮质畸形正在受到越来越多的关注，但是 他们的病因和意义尚不清楚。 我们已经看到它们是 与至少一种学习障碍形式有关 - 发展 阅读障碍。 我们希望这项研究将阐明 皮质畸形及其对行为的可能后果。