Sjöbeck M, Englund E
Division of Neuropathology, Department of Pathology and Cytology, University Hospital, Lund, Sweden.
Dement Geriatr Cogn Disord. 2001 May-Jun;12(3):211-8. doi: 10.1159/000051260.
Structural manifestations of Alzheimer's disease (AD) including neuronal loss were investigated in 12 cases of AD and in 10 healthy age-matched controls, with focus on the cerebellum. Linear Purkinje cell (PC) density was measured in the vermis and cerebellar hemispheres. Neurons were also counted in the inferior olivary nucleus. In vermis of the AD cases, the mean PC number was significantly lower (p = 0.019) than in the controls. The neurons in the inferior olive were similarly fewer, though not significantly (p = 0.13). Molecular layer gliosis and atrophy in the vermis was clearly severer in AD than in the controls. Features typical of cerebral Alzheimer encephalopathy (plaques, tangles and microvacuolization) were inconspicious. The structural cerebellar changes in the AD cases were thus neuronal loss, atrophy and gliosis, judged to represent the disease process, and with a main involvement in the vermis. This may be reflected in some of the symptoms and signs seen in AD, signs that are generally overlooked or judged to be of noncerebellar origin.
在12例阿尔茨海默病(AD)患者和10例年龄匹配的健康对照者中,研究了包括神经元丢失在内的AD结构表现,重点关注小脑。测量了蚓部和小脑半球的线性浦肯野细胞(PC)密度。还对下橄榄核中的神经元进行了计数。在AD病例的蚓部,平均PC数量显著低于对照组(p = 0.019)。下橄榄核中的神经元数量同样较少,尽管差异不显著(p = 0.13)。AD患者蚓部的分子层胶质细胞增生和萎缩明显比对照组严重。典型的脑阿尔茨海默病脑病特征(斑块、缠结和微空泡化)不明显。因此,AD病例中的小脑结构变化为神经元丢失、萎缩和胶质细胞增生,被认为代表了疾病过程,且主要累及蚓部。这可能反映在AD中出现的一些症状和体征上,这些症状和体征通常被忽视或被认为起源于非小脑。