Arendt T, Brückner M K, Bigl V, Marcova L
Department of Neurochemistry, Paul Flechsig Institute of Brain Research, University of Leipzig, Germany.
J Comp Neurol. 1995 Jan 9;351(2):189-222. doi: 10.1002/cne.903510203.
Changes in the dendritic arborisation of Golgi-impregnated basal forebrain neurones with respect to size, shape, orientation, and topology of branching were quantitatively investigated in ageing, Alzheimer's disease (AD), Korsakoff's disease (KD), and Parkinson's disease (PD). A reorganisation of the whole dendritic tree characterized by an increase in both the total dendritic length and the degree of dendritic arborisation as well as by changes in the shape of the dendritic field was found during ageing, in KD, PD, and AD. Dendritic growth under these conditions was related to the extent of cell loss in basal forebrain nuclei. There appeared to be major differences, however, with respect to the overall pattern of dendritic reorganisation between AD on one side and ageing, KD, and PD on the other side. In both ageing and KD, dendritic growth was largely restricted to the terminal dendritic segments, resulting in an increase of the size of the dendritic field (pattern of "extensive growth") In AD, however, dendritic growth mainly resulted in an increase of the dendritic density within the dendritic field without being accompanied by an increase in the size of the volume occupied by the dendritic tree (pattern of "intensive growth"). In AD, aberrant growth processes were frequently observed in the perisomatic area or on distal dendritic segments of basal forebrain neurones of the reticular type. Neurones with aberrant growth profiles were typically located in the direct vicinity of deposits of beta/A4 amyloid. Perisomatic growth profiles were covered by the low-affinity receptor of nerve growth factor p75NGFR. Aberrant growth processes were not present in ageing, KD, and PD. On the basis of the present study, it is concluded that under certain degenerative conditions, reticular basal forebrain neurones undergo a compensatory reorganisation of their dendritic arborisation, a process that has become defective in AD, thereby converting a physiological signal into a cascade of events contributing to the pathology of the disease.
在衰老、阿尔茨海默病（AD）、科萨科夫综合征（KD）和帕金森病（PD）中，对经高尔基染色法处理的基底前脑神经元树突分支在大小、形状、方向和分支拓扑结构方面的变化进行了定量研究。在衰老、KD、PD和AD过程中，发现整个树突树发生了重组，其特征是总树突长度和树突分支程度增加，以及树突野形状发生变化。在这些情况下，树突生长与基底前脑核中的细胞丢失程度有关。然而，AD与衰老、KD和PD在树突重组的总体模式方面似乎存在主要差异。在衰老和KD中，树突生长主要局限于树突末端节段，导致树突野大小增加（“广泛生长”模式）。然而，在AD中，树突生长主要导致树突野内树突密度增加，而树突树所占体积大小并未增加（“密集生长”模式）。在AD中，常在网状型基底前脑神经元的胞体周围区域或树突远端节段观察到异常生长过程。具有异常生长特征的神经元通常位于β/A4淀粉样蛋白沉积物的直接附近。胞体周围的生长特征被神经生长因子p75NGFR的低亲和力受体覆盖。在衰老、KD和PD中不存在异常生长过程。基于本研究，得出结论：在某些退行性条件下，网状基底前脑神经元经历其树突分支的代偿性重组，这一过程在AD中出现缺陷，从而将生理信号转化为一系列导致疾病病理的事件。
