Roberts G W, Gentleman S M, Lynch A, Murray L, Landon M, Graham D I
Smith Kline Beecham Pharmaceuticals, Harlow, UK.
J Neurol Neurosurg Psychiatry. 1994 Apr;57(4):419-25. doi: 10.1136/jnnp.57.4.419.
In a recent preliminary study it was reported that a severe head injury resulted in the deposition of beta amyloid protein (beta AP) in the cortical ribbon of 30% of patients who survived for less than two weeks. Multiple cortical areas have now been examined from 152 patients (age range 8 weeks-81 years) after a severe head injury with a survival time of between four hours and 2.5 years. This series was compared with a group of 44 neurologically normal controls (age range 51 to 80 years). Immunostaining with an antibody to beta AP confirmed the original findings that 30% of cases of head injury have beta AP deposits in one or more cortical areas. Increasing age seemed to accentuate the extent of beta AP deposition and potential correlations with other pathological changes associated with head injury were also investigated. In addition, beta amyloid precursor protein (beta APP) immunoreactivity was increased in the perikarya of neurons in the vicinity of beta AP deposits. The data from this study support proposals that increased expression of beta APP is part of an acute phase response to neuronal injury in the human brain, that extensive overexpression of beta APP can lead to deposition of beta AP and the initiation of an Alzheimer disease-type process within days, and that head injury may be an important aetiological factor in Alzheimer's disease.
在最近一项初步研究中，据报道，严重颅脑损伤导致30%存活时间不到两周的患者皮质带中出现β淀粉样蛋白（β-AP）沉积。现已对152例严重颅脑损伤患者（年龄范围8周 - 81岁）的多个皮质区域进行了检查，这些患者的存活时间在4小时至2.5年之间。该系列患者与44名神经功能正常的对照组（年龄范围51至80岁）进行了比较。用抗β-AP抗体进行免疫染色证实了最初的发现，即30%的颅脑损伤病例在一个或多个皮质区域有β-AP沉积。年龄增长似乎会加重β-AP沉积的程度，并且还研究了其与颅脑损伤相关的其他病理变化的潜在相关性。此外，在β-AP沉积附近的神经元胞体中，β淀粉样前体蛋白（β-APP）的免疫反应性增加。这项研究的数据支持以下观点：β-APP表达增加是人类大脑对神经元损伤急性期反应的一部分，β-APP的广泛过度表达可导致β-AP沉积，并在数天内引发阿尔茨海默病类型的进程，而且颅脑损伤可能是阿尔茨海默病的一个重要病因。
