Cerebral amyloid beta protein deposits and other Alzheimer lesions in non-demented elderly east Africans.
Cerebral amyloid beta protein deposits and other Alzheimer lesions in non-demented elderly east Africans.
复制标题
非痴呆老年东非人的大脑β淀粉样蛋白沉积物和其他阿尔茨海默病病变。
DOI：
10.1111/j.1750-3639.1996.tb00790.x
复制
发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Kalaria,RN
中科院分区：
文献类型：
--
作者：
Ogeng'o,JA;Cohen,DL;Sayi,JG;Matuja,WB;Chande,HM;Kitinya,JN;Kimani,JK;Friedland,RP;Mori,H;Kalaria,RN
人们对发展中国家土著居民中阿尔茨海默病（AD）或阿尔茨海默型痴呆的存在知之甚少。为了评估这一点，我们评估了老年东非人大脑中β淀粉样蛋白（Aβ）的沉积和其他与AD相关的病变。在内罗毕和达累斯萨拉姆的两家医疗机构进行尸检的32名受试者的脑组织进行了检查，他们的年龄在45岁至83岁之间，没有明显的神经系统疾病。从克利夫兰因类似原因死亡的受试者中选取年龄匹配的样本进行平行评估。在来自内罗毕的20个样本中，3个（15%）大脑显示新皮质Aβ沉积，从大量弥漫性斑块到高度局部的致密斑块或神经性斑块不等，其中许多也是硫黄素S阳性。其中2例在前额叶和颞叶皮层有深度AS沉积，其中1例还表现出中度至重度脑淀粉样血管病。同样，来自达累斯萨拉姆的12个样品中有2个样品显示出弥漫性和致密的Aβ沉积物，与Aβ40相比，这些沉积物对较长的Aβ42物种也具有主要的反应性。我们还注意到，Aβ斑块对淀粉样蛋白相关蛋白、载脂蛋白E、血清淀粉样蛋白P和补体C3具有不同的免疫反应。4名受试者海马中也有明显的Tau蛋白反应性神经原纤维缠结（NFT）。相比之下，在克利夫兰随机选择的20个尸检样本中，有4个（20%）在弥漫性和致密性实质斑块和脉管系统中发现了Aβ沉积。这些观察结果表明，非痴呆的东非人大脑中的Aβ沉积和一些NFT在质量和数量上与来自克利夫兰的年龄匹配的老年人对照组相似。虽然我们的小规模研究没有记录类似的临床前阿尔茨海默病患病率，但它表明东非老年人不太可能像发达国家所知的那样逃脱阿尔茨海默病。
There is little knowledge of the existence of Alzheimer disease (AD) or Alzheimer type of dementia in indigenous populations of developing countries. In an effort to evaluate this, we assessed the deposition of amyloid β (Aβ) protein and other lesions associated with AD in brains of elderly East Africans. Brain tissues were examined from 32 subjects, aged 45 to 83 years with no apparent neurological disease, who came to autopsy at two medical Institutions in Nairobi and Dar es Salaam. An age‐matched sample from subjects who had died from similar causes in Cleveland was assessed in parallel. Of the 20 samples from Nairobi, 3 (15%) brains exhibited neocortical Aβ deposits that varied from numerous diffuse to highly localized compact or neuritic plaques, many of which were also thioflavin S positive. Two of the cases had profound AS deposition in the prefrontal and temporal cortices and one of these also exhibited moderate to severe cerebral amyloid angiopathy. Similarly, 2 of the 12 samples from Dar es Salaam exhibited diffuse and compact Aβ deposits that were also predominantly reactive for the longer Aβ42species compared to Aβ40. We also noted that Aβ plaques were variably immunoreactive for amyloid associated proteins, apolipoprotein E, serum amyloid P and complement C3. Tau protein reactive neurofibrillary tangles (NFT) were also evident in the hippocampus of 4 subjects. By comparison, 4 (20%) of the 20 samples from randomly selected autopsies performed in Cleveland showed Aβ deposits within diffuse and compact parenchymal plaques and the vasculature. These observations suggest Aβ deposition and some NFT in brains of non‐demented East Africans are qualitatively and quantitatively similar to that in age‐matched elderly controls from Cleveland. While our small scale study does not document similar prevalence rates of preclinical AD, it suggests that elderly East Africans are unlikely to escape AD as it is known in developed countries.