CEREBRAL WHITE-MATTER CHANGES IN ACQUIRED-IMMUNODEFICIENCY-SYNDROME DEMENTIA - ALTERATIONS OF THE BLOOD-BRAIN-BARRIER
CEREBRAL WHITE-MATTER CHANGES IN ACQUIRED-IMMUNODEFICIENCY-SYNDROME DEMENTIA - ALTERATIONS OF THE BLOOD-BRAIN-BARRIER
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DOI：
10.1002/ana.410340307
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发表时间：
1993-09-01
影响因子：
11.2
通讯作者：
TRAPP, BD
中科院分区：
文献类型：
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作者：
POWER, C;KONG, PA;TRAPP, BD
获得性免疫缺陷综合征（AIDS）痴呆是人类免疫缺陷病毒（HIV）感染的常见晚期表现，其病因尚不清楚，但放射学和病理学研究表明皮质下白色物质发生改变。 为了研究这些白色物质异常的病理基础，我们对患有和不患有痴呆的艾滋病患者、艾滋病前期患者（无症状艾滋病毒血清阳性患者）和艾滋病毒血清阴性对照受试者的皮质下白色物质进行了免疫细胞化学和组织学分析。在15名AIDS痴呆患者中的8名、13名AIDS非痴呆患者中的3名中检测到Luxol固蓝染色强度降低，称为“弥漫性髓鞘苍白”，而在AIDS前患者（n = 2）或对照受试者（n = 9）中均未检测到。与Luxol坚牢蓝染色相反，髓鞘蛋白免疫细胞化学染色的切片在弥漫性髓鞘苍白的区域中没有显示染色强度降低。此外，无论是脱髓鞘轴突或主动脱髓鞘检测在光和电子显微镜下的皮质下白色物质从艾滋病痴呆患者的大脑。在HIV感染患者的脑切片中，血管周围巨噬细胞数量增加，星形胶质细胞和小胶质细胞肥大。这些变化并非痴呆或弥漫性髓鞘苍白区域所特有，它们发生在灰质和白色物质中。在12例AIDS痴呆患者和6例AIDS非痴呆患者的脑中，白色胶质细胞中的血清蛋白明显积聚，与AIDS痴呆患者脑中髓鞘病理学的缺乏相反。在12例AIDS痴呆患者中的11例和12例非痴呆AIDS患者中的3例的额叶皮质中检测到血清蛋白免疫阳性神经元。血清阴性对照受试者在皮质和白色物质中均显示极轻微的血清蛋白免疫反应性。因此，我们得出结论，血脑屏障的改变，而不是脱髓鞘有助于艾滋病痴呆的发展。
The cause of acquired immunodeficiency syndrome (AIDS) dementia, which is a frequent late manifestation of human immunodeficiency virus (HIV) infection, is unknown but radiological and pathological studies have implicated alterations in subcortical white matter. To investigate the pathological basis of these white matter abnormalities, we performed an immunocytochemical and histological analysis of subcortical white matter from AIDS patients with and without dementia, from pre-AIDS patients (asymptomatic HIV-seropositive patients), and from HIV-seronegative control subjects. Reduced intensity of Luxol fast blue staining, designated ''diffuse myelin pallor,'' was detected in 8 of 15 AIDS dementia patients, 3 of 13 AIDS nondemented patients, and none of the pre-AIDS patients (n = 2) or control subjects (n = 9). In contrast to Luxol fast blue staining, sections stained immunocytochemically for myelin proteins did not show decreased staining intensities in regions of diffuse myelin pallor. In addition, neither demyelinated axons nor active demyelination were detected in light and electron micrographs of subcortical white matter from brains of patients with AIDS dementia. An increase in the number of perivascular macrophages and hypertrophy of astrocytes and microglia occurred in brain sections from HIV-infected patients. These changes were not specific to dementia or regions of diffuse myelin pallor and they occurred in both gray and white matter. In contrast to the lack of myelin pathology in AIDS dementia brains, significant accumulations of serum proteins in white matter glia were detected in the brains of 12 of 12 patients with AIDS dementia and 6 of 12 AIDS patients without dementia. Serum protein-immunopositive cortical neurons were detected in the frontal cortex of 11 of 12 patients with AIDS dementia and 3 of 12 nondemented AIDS patients. Seronegative control subjects showed minimal serum protein immunoreactivity in both cortex and white matter. We conclude therefore that alterations in the blood-brain barrier and not demyelination contribute to the development of AIDS dementia.