Reorganization of cingulate cortex in Alzheimer's disease: neuron loss, neuritic plaques, and muscarinic receptor binding.
Reorganization of cingulate cortex in Alzheimer's disease: neuron loss, neuritic plaques, and muscarinic receptor binding.
复制标题
阿尔茨海默病中扣带皮层的重组：神经元丢失、神经炎斑块和毒蕈碱受体结合。
DOI：
10.1093/cercor/2.6.526
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Vogt,LJ
中科院分区：
文献类型：
--
作者：
Vogt,BA;Crino,PB;Vogt,LJ
Pathology related to dementia of the Alzheimer type (DAT) develops later in cingulate cortex than in medial temporal areas. Therefore, end-stage cases have earlier forms of pathology in cingulate cortex, and postmortem studies of this region may provide a window on processes that temporal cortices pass through decades before death. Five classes of DAT have been described on the basis of neuron degeneration and receptor binding in posterior cingulate cortex. The present study assessed binding of3H-oxotremorine-M with pirenzepine (OXO-M/PZ), a protocol for presynaptic muscarinic receptors, and thioflavin S-stained neuritic plaques (NPs) in cingulate area 23a in 12 DAT cases distributed over four classes of pathology and in nine age-matched control cases. OXO-M/PZ binding was significantly elevated in layers I, II, IV, and VI of all DAT cases and was very high in layer V compared to control cases. Almost 75% of the layer Va increase was due to binding in classes 2 and 3, while classes 1 and 4 were least affected. In class 3 cases, neuron density in layer Va was inversely correlated with OXO-M/PZ binding (r = -0.98) and primitive NP densities (r = -0.93). The close association between neuron densities and presynaptic muscarinic ligand binding in some classes confirms that there are independent classes of DAT. The high and inverse correlations between cortical pathology and ligand binding in class 3 cases suggest that there is a progression in class 3 pathology. Finally, elevated OXO-M/PZ binding and a report of increased choline uptake suggest that cholinergic axons sprout in DAT, and this sprouting may be associated with a progressive loss of postsynaptic elements.
