ALZHEIMERS DISEASE-LIKE DYSTROPHIC NEURITES CHARACTERISTICALLY ASSOCIATED WITH SENILE PLAQUES ARE NOT FOUND WITHIN OTHER NEURODEGENERATIVE DISEASES UNLESS AMYLOID BETA-PROTEIN DEPOSITION IS PRESENT
ALZHEIMERS DISEASE-LIKE DYSTROPHIC NEURITES CHARACTERISTICALLY ASSOCIATED WITH SENILE PLAQUES ARE NOT FOUND WITHIN OTHER NEURODEGENERATIVE DISEASES UNLESS AMYLOID BETA-PROTEIN DEPOSITION IS PRESENT
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DOI：
10.1016/0006-8993(93)91563-8
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发表时间：
1993-03-19
期刊：
影响因子：
2.9
通讯作者：
ARMSTRONG, DM
中科院分区：
文献类型：
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作者：
BENZING, WC;MUFSON, EJ;ARMSTRONG, DM
swellous，球根状（营养不良）神经突是阿尔茨海默病（AD）的常见病理特征，并代表了最丰富的神经炎异常内患有这种疾病的患者的大脑。在本研究中，我们试图确定与老年斑相关的营养不良性神经突是否是AD所特有的，或者它们是否是在其他神经退行性疾病中可以观察到的更普遍的神经炎和/或神经元变性过程的特征。为了实现这一点，我们检查了AD、帕金森病（PD）、帕金森病伴AD、帕金森病伴痴呆但无AD病理、亨廷顿病（HD）、皮克病和正常年龄匹配对照（NC）患者的死后脑材料。使用一组针对淀粉样β蛋白（A β P）、成对螺旋丝（PHF）、酪氨酸羟化酶、P物质、神经降压素和生长抑素的抗体，我们发现AD中典型的免疫标记营养不良性神经突仅见于A β P沉积的病例和脑区。更具体地说，已知显示严重传入和/或局部退行性变化的大脑区域，如所有三个PD组中的尾状核和壳核，HD病例中的尾状核，以及HD和Pick病例中的颞叶皮质，明显没有这些肿胀的神经突，除非还存在A β P沉积。虽然这些发现并不排除其他形式的神经炎变性可能伴随着这些其他疾病中观察到的变性的可能性，但它们确实表明，在AD大脑中经常观察到的扩大的免疫标记神经突是AD所特有的，特别是仅限于具有β淀粉样蛋白沉积的大脑区域。
Swollen, bulbous-shaped (dystrophic) neurites are a common pathologic feature of Alzheimer's disease (AD) and represent one of the most abundant neuritic abnormalities within the brains of patients with this disease. In the present study, we sought to determine whether the dystrophic neurites which are observed in association with senile plaques are unique to AD or whether they are characteristic of a more generalized process of neuritic and/or neuronal degeneration which can be observed in other neurodegenerative diseases. To accomplish this, we examined post-mortem brain material from patients with AD, Parkinson's disease (PD), Parkinson's disease with associated AD, Parkinson's disease with dementia yet without AD pathology, Huntington's disease (HD), Pick's disease and normal age-matched controls (NC). Using a battery of antibodies to amyloid beta-protein (AbetaP), paired-helical filaments (PHF), tyrosine hydroxylase, substance P, neurotensin, and somatostatin we found that immunolabeled dystrophic neurites of the type characteristically observed in AD, were seen only in cases and in brain regions where AbetaP deposition was present. More specifically, brain areas known to display severe afferent and/or local degenerative changes such as the caudate and putamen in all three PD groups, the caudate in the HD cases, and the temporal cortex in the HD and Pick's cases were conspicuously free of these swollen neurites unless AbetaP deposition was also present. While these findings did not exclude the possibility that other forms of neuritic degeneration may accompany the degeneration seen in these other diseases, they do suggest that the enlarged immunolabeled neurites so frequently observed in AD brains are unique to AD and in particular are restricted to brain regions with beta-amyloid deposits.