Perry T L, Yong V W, Bergeron C, Hansen S, Jones K
Ann Neurol. 1987 Apr;21(4):331-6. doi: 10.1002/ana.410210403.
We measured the contents of amino acids and related amino compounds in autopsied brain from 22 patients with Alzheimer's disease (AD) and in cortical biopsy specimens from 2 other patients. The diagnosis of AD was established neuropathologically in all 24 patients by the presence of both neurofibrillary tangles and neuritic plaques in neocortex. The mean contents of gamma-aminobutyric acid (GABA), and of the GABA dipeptide homocarnosine, were significantly reduced in frontal and occipital cortices and in hippocampus of the autopsied brains of AD patients compared to control patients without neurological disease. However, GABA contents were normal in frontal cortex in biopsy samples from 2 patients. Phosphoethanolamine contents were significantly reduced at autopsy in frontal and occipital cortex, and in the substantia innominata. We found no evidence of a deficiency of glutamate, aspartate, or taurine in AD brain, as has been claimed. Glutathione contents and glutathione transferase activities were normal in frontal cortex and substantia innominata. The mechanism of neuronal death in patients with AD is unlikely to involve either insufficient synthesis of glutathione or failure to conjugate free radicals with glutathione.
我们测定了22例阿尔茨海默病（AD）患者尸检大脑以及另外2例患者皮质活检标本中的氨基酸及相关氨基化合物的含量。通过新皮质中同时存在神经原纤维缠结和神经炎斑块，对所有24例患者进行了AD的神经病理学诊断。与无神经系统疾病的对照患者相比，AD患者尸检大脑额叶、枕叶皮质及海马中γ-氨基丁酸（GABA）和GABA二肽高肌肽的平均含量显著降低。然而，2例患者活检样本的额叶皮质中GABA含量正常。尸检时额叶、枕叶皮质及无名质中的磷酸乙醇胺含量显著降低。我们未发现如所声称的AD大脑中谷氨酸、天冬氨酸或牛磺酸缺乏的证据。额叶皮质和无名质中的谷胱甘肽含量及谷胱甘肽转移酶活性正常。AD患者神经元死亡的机制不太可能涉及谷胱甘肽合成不足或自由基与谷胱甘肽结合失败。
