Sherman G F, Galaburda A M, Behan P O, Rosen G D
Dyslexia Research Laboratory, Charles A. Dana Research Institute, Beth Israel Hospital, Boston, MA 02215.
Acta Neuropathol. 1987;74(3):239-42. doi: 10.1007/BF00688187.
The cerebral cortex was examined for signs of pathology in the NZB, BXSB, and MRL autoimmune strains of mice, crosses among these strains, and control mice. Previously, we reported that 20% of NZB mice had ectopic collections of neurons in layer I of the cortex. In this study we replicated this finding in the NZB, and extended it to the BXSB strain, and BXSB/NZB and MRL/NZB hybrids. The MRL strain, however, did not have a large number of individuals with brain anomalies. Thus, a number of autoimmune mice strains and hybrids develop brain anomalies, although at least one autoimmune strain does not. We suggest that in certain autoimmune strains maternal autoantibodies cross the placenta and damage the developing fetal brain, and that these strains may be useful experimental models for studying the development of brain anomalies seen in the dyslexic human.
对新西兰黑鼠（NZB）、BXSB和MRL自身免疫品系小鼠、这些品系之间的杂交后代以及对照小鼠的大脑皮层进行了病理学迹象检查。此前，我们报告称20%的NZB小鼠在皮层I层有神经元异位聚集。在本研究中，我们在NZB小鼠中重复了这一发现，并将其扩展至BXSB品系以及BXSB/NZB和MRL/NZB杂交后代。然而，MRL品系中没有大量个体存在脑异常。因此，尽管至少有一种自身免疫品系没有，但许多自身免疫小鼠品系和杂交后代会出现脑异常。我们认为，在某些自身免疫品系中，母源自身抗体穿过胎盘并损害发育中的胎儿大脑，并且这些品系可能是研究诵读困难人群中所见脑异常发育的有用实验模型。
