Wirths O, Weickert S, Majtenyi K, Havas L, Kahle P J, Okochi M, Haass C, Multhaup G, Beyreuther K, Bayer T A
Department of Psychiatry, University of Bonn Medical Center, Germany.
Neuroreport. 2000 Nov 27;11(17):3737-41. doi: 10.1097/00001756-200011270-00029.
The contribution of alpha-synuclein accumulation in Alzheimer's disease (AD) plaques is currently a matter of scientific debate. In the present study antisera against the N- and C-terminus, the full-length protein and the central so-called non-amyloid component (NAC) domain of the alpha-synuclein protein were used to address this question in brains of cases with typical AD and of cases with the Lewy body (LB) variant of AD. In typical AD cases, none of the antisera revealed evidence for co-accumulation of alpha-synuclein with extracellular A beta peptides in plaques or in dystrophic neurites decorating the plaque core. Interestingly, cases with mixed pathology of the LB variant of AD revealed accumulation of alpha-synuclein in LBs and in dystrophic neurites of A beta plaques.
α-突触核蛋白在阿尔茨海默病（AD）斑块中的作用目前是一个科学争论的问题。在本研究中，针对α-突触核蛋白的N端和C端、全长蛋白以及所谓的中央非淀粉样成分（NAC）结构域的抗血清，被用于在典型AD病例以及AD路易体（LB）变异型病例的大脑中解决这个问题。在典型AD病例中，没有一种抗血清显示α-突触核蛋白与细胞外Aβ肽在斑块中或在装饰斑块核心的营养不良性神经突中共积累的证据。有趣的是，AD的LB变异型混合病理病例显示α-突触核蛋白在路易体和Aβ斑块的营养不良性神经突中积累。
