Wetterling T, Tegtmeyer K F
Klinik für Psychiatrie, Medizinische Universität Lübeck, Germany.
Clin Investig. 1994 Feb;72(3):196-9. doi: 10.1007/BF00189310.
The deposition of beta A4-amyloid in senile plaques and small cerebral vessels is one of the pathological hallmarks of Alzheimer's disease. Recent data suggest that protease inhibitors such as alpha 2-macroglobulin may be involved in the process of forming beta A4 amyloid deposits. Compared to 34 persons without neurological diseases, the serum content of alpha 1-antitrypsin was increased in 16 patients with Alzheimer's disease and 15 with Binswanger's disease. In the latter alpha 2-macroglobulin was also elevated in serum. Our results show no evidence of a blood-borne origin of the protein or peptid deposited in the walls of small vessels in Alzheimer's or Binswanger's disease. Nevertheless, the elevated proteinase inhibitor concentrations may play a role in the pathogenesis of these diseases.
βA4淀粉样蛋白在老年斑和脑小血管中的沉积是阿尔茨海默病的病理特征之一。最近的数据表明,诸如α2-巨球蛋白等蛋白酶抑制剂可能参与βA4淀粉样蛋白沉积物的形成过程。与34名无神经疾病的人相比,16名阿尔茨海默病患者和15名宾斯旺格病患者的血清α1-抗胰蛋白酶含量增加。在后者中,血清α2-巨球蛋白也升高。我们的结果没有显示在阿尔茨海默病或宾斯旺格病小血管壁中沉积的蛋白质或肽有血源性起源的证据。然而,蛋白酶抑制剂浓度升高可能在这些疾病的发病机制中起作用。