McGeer P L, McGeer E G
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada.
Ann N Y Acad Sci. 1996 Jan 17;777:213-20. doi: 10.1111/j.1749-6632.1996.tb34421.x.
Lesions in Alzheimer disease are characterized by the assembly of a variety of cells and proteins associated with the immune system. Activated microglia express high levels of MHC glycoproteins and receptors for complement. Small numbers of T-lymphocytes infiltrate tissue. Proteins of the classical complement pathway are closely connected with beta-amyloid deposits. Several materials associated with senile plaques, including beta-amyloid protein itself, bind C1q in vitro and activate the pathway. The membrane attack complex of complement, as well as proteins which defend against that complex, colocalize with dystrophic neurites. These data imply that an autodestructive process is occurring in Alzheimer's disease, and that anti-inflammatory drugs might be an effective form of therapy. Some epidemiological evidence and results of a pilot clinical trial support this hypothesis.
阿尔茨海默病的病变特征是多种与免疫系统相关的细胞和蛋白质聚集。活化的小胶质细胞表达高水平的MHC糖蛋白和补体受体。少量T淋巴细胞浸润组织。经典补体途径的蛋白质与β-淀粉样蛋白沉积密切相关。几种与老年斑相关的物质，包括β-淀粉样蛋白本身，在体外与C1q结合并激活该途径。补体的膜攻击复合物以及抵御该复合物的蛋白质与营养不良性神经突共定位。这些数据表明，阿尔茨海默病正在发生自毁过程，抗炎药物可能是一种有效的治疗形式。一些流行病学证据和一项初步临床试验的结果支持这一假设。
