Department of Neurology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Switzerland.
Department of Internal Medicine, Rehabilitation and Geriatrics, Geneva University Hospitals and Faculty of Medicine, Switzerland.
J Alzheimers Dis. 2014;39(1):115-20. doi: 10.3233/JAD-131289.
About one third of Alzheimer's disease (AD) patients develop some parkinsonian features, yet half of them do not have Lewy body pathology at autopsy. The neuropathological substrate of parkinsonism in AD is still unclear. In the present study, we measured neuronal and neurofibrillary tangles (NFTs) densities in the substantia nigra pars compacta (SN) and in the putamen of 22 AD patients, 11 with and 11 without parkinsonism, here defined as the presence of bradykinesia and at least one of resting tremor, rigidity, or gait disorders. Our study showed that parkinsonism associated with AD was related to a significant loss of neurons both in the SN and in the putamen, suggesting pre-and postsynaptic alterations of the nigrostriatal pathway. Neuronal tau deposition was a less important factor as density of NFTs correlated with parkinsonism only in the SN but not in the putamen. We propose that a subgroup of pure AD patients develop parkinsonian symptoms as a result of neuronal loss in the basal ganglia, indicating a prominent subcortical involvement, which appears unrelated to the Braak stage of AD.
约三分之一的阿尔茨海默病（AD）患者出现一些帕金森特征，但其中一半在尸检时没有路易体病理学。AD 中帕金森病的神经病理学基础仍不清楚。在本研究中，我们测量了 22 名 AD 患者（11 名伴发和 11 名不伴发帕金森病）黑质致密部（SN）和纹状体神经元和神经原纤维缠结（NFTs）的密度，帕金森病在这里定义为存在运动迟缓，以及静止性震颤、僵硬或步态障碍至少一项。我们的研究表明，与 AD 相关的帕金森病与 SN 和纹状体中神经元的显著丧失有关，这表明黑质纹状体通路的突触前和突触后改变。神经元tau 沉积是一个不太重要的因素，因为 NFTs 的密度仅与 SN 中的帕金森病相关，而与纹状体无关。我们提出，一小部分纯 AD 患者由于基底节神经元丧失而出现帕金森症状，表明存在明显的皮质下受累，这与 AD 的 Braak 分期无关。
