Bayer T A, Jäkälä P, Hartmann T, Havas L, McLean C, Culvenor J G, Li Q X, Masters C L, Falkai P, Beyreuther K
Department of Psychiatry, University of Bonn Medical Center, Germany.
Neurosci Lett. 1999 May 14;266(3):213-6. doi: 10.1016/s0304-3940(99)00311-0.
A growing body of evidence suggests that the non-Abeta component of Alzheimer's disease amyloid precursor protein (NACP) or alpha-synuclein contributes to the neurodegenerative processes in Alzheimer's disease (AD), Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In the present study antisera to the N terminus and the NAC domain of the alpha-synuclein protein were employed to elucidate the expression pattern in brains of patients with AD, PD, DLB and control specimen. Alpha-synuclein exhibited an overall punctuate expression profile compatible with a synaptic function. Interestingly, while Lewy bodies were strongly immunoreactive, none of the alpha-synuclein antisera revealed staining in mature beta-amyloid plaques in AD. These observations suggest that alpha-synuclein does not contribute to late neurodegenerative processes in AD brains.
越来越多的证据表明,阿尔茨海默病淀粉样前体蛋白(NACP)的非Aβ成分或α-突触核蛋白参与了阿尔茨海默病(AD)、帕金森病(PD)和路易体痴呆(DLB)的神经退行性过程。在本研究中,使用针对α-突触核蛋白N端和NAC结构域的抗血清来阐明AD、PD、DLB患者大脑以及对照样本中的表达模式。α-突触核蛋白呈现出与突触功能相符的整体点状表达谱。有趣的是,虽然路易体具有强烈的免疫反应性,但在AD患者成熟的β-淀粉样斑块中,没有一种α-突触核蛋白抗血清显示出染色。这些观察结果表明,α-突触核蛋白不参与AD大脑中的晚期神经退行性过程。