Adams I M
Department of Science, Edith Cowan University, Joondalup, Australia.
Mol Neurobiol. 1991;5(2-4):411-9. doi: 10.1007/BF02935562.
Plasticity of the synaptic contact zone was previously observed following loss of synapses in the cerebral cortex of normal aging humans. The present study was undertaken to determine if there was quantitative evidence of synapse loss and synapse plasticity in the inferior temporal, superior parietal, parieto-occipital, and superior frontal cortical regions in Alzheimer's disease (AD), and how such changes related to the neurofibrillary tangles and amyloid plaques. The results showed that age at autopsy did not correlate with the numbers of synapses, plaques, or tangles. However, the numbers of synapses strongly reflected the pathology of AD; in all four brain regions, there were fewer synapses as the numbers of plaques and tangles increased. In the inferior temporal and superior parietal cortices, the loss of synapses was accompanied by an increase in the synaptic contact length. The results suggest that, in some cerebral cortical brain regions, synapses are capable of plasticity changes, even when the pathology of AD and loss of synapses are severe.
先前在正常衰老人类的大脑皮质突触丧失后观察到突触接触区的可塑性。本研究旨在确定在阿尔茨海默病(AD)的颞下回、顶上叶、顶枕叶和额上回皮质区域是否存在突触丧失和突触可塑性的定量证据,以及这些变化如何与神经原纤维缠结和淀粉样斑块相关。结果显示,尸检年龄与突触、斑块或缠结的数量无关。然而,突触数量强烈反映了AD的病理情况;在所有四个脑区,随着斑块和缠结数量的增加,突触数量减少。在颞下回和顶上叶皮质,突触丧失伴随着突触接触长度的增加。结果表明,在某些大脑皮质脑区,即使AD病理和突触丧失严重,突触仍能够发生可塑性变化。