Gsell W, Conrad R, Hickethier M, Sofic E, Frölich L, Wichart I, Jellinger K, Moll G, Ransmayr G, Beckmann H
Department of Psychiatry, University of Würzburg, Germany.
J Neurochem. 1995 Mar;64(3):1216-23. doi: 10.1046/j.1471-4159.1995.64031216.x.
"Oxidative stress" may be of significance in the etiopathogenesis of dementia of Alzheimer type (DAT). Therefore, we measured activities of the enzymes superoxide dismutase (SOD) and catalase (CAT), which detoxicate reactive oxygen species. Enzyme activities were measured postmortem in basal ganglia, cortical, and limbic brain regions of patients with DAT and age-matched controls. SOD activity increased with age in basal nucleus of Meynert. However, there was no significant difference in SOD activity between DAT and controls. CAT activity was independent of age and postmortem time. There were significant reductions in CAT activity in parietotemporal cortex, basal ganglia, and amygdala in DAT compared with controls (p < 0.05 to 0.01). Our findings are in line with the assumption that reactive oxygen species could contribute to the pathogenesis of DAT. Absence of these changes in basal nucleus of Meynert might reflect retrograde degeneration of cholinergic fibers.
“氧化应激”可能在阿尔茨海默病型痴呆（DAT）的病因发病机制中具有重要意义。因此，我们测量了超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，这两种酶可清除活性氧。在患有DAT的患者和年龄匹配的对照组的基底神经节、皮质和边缘脑区进行了死后酶活性测量。在Meynert基底核中，SOD活性随年龄增加。然而，DAT患者和对照组之间的SOD活性没有显著差异。CAT活性与年龄和死后时间无关。与对照组相比，DAT患者的顶颞叶皮质、基底神经节和杏仁核中的CAT活性显著降低（p<0.05至0.01）。我们的研究结果符合活性氧可能导致DAT发病机制的假设。Meynert基底核中没有这些变化可能反映了胆碱能纤维的逆行性变性。
