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目前有很多关于AD发病机制的假说,但现在被接受的是Αβ级联反应假说、即Αβ42产生过多、而降解减少,致Αβ42总量增加、并形成可溶性稳定的寡聚体,影响谷氨酸后突触神经元的突触功能,即影响突触可塑性为始动因素。
于挺敏教授:睡眠性头痛研究进展
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