Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, CA 90095-1732, USA.
J Neurosci Res. 2010 Aug 1;88(10):2083-90. doi: 10.1002/jnr.22392.
Synaptic transmission is essential for nervous system function, and its dysfunction is a known major contributing factor to Alzheimer's-type dementia. Antigen-specific immunochemical methods are able to characterize synapse loss in dementia through the quantification of various synaptic proteins involved in the synaptic cycle. These immunochemical methods applied to the study of Alzheimer's disease (AD) brain specimens have correlated synaptic loss with particularly toxic forms of amyloid-beta protein and have also established synapse loss as the best correlate of dementia severity. A significant but comparatively circumscribed amount of literature describes synaptic decline in other forms of dementia. Ischemic vascular dementia (IVD) is quite heterogeneous, and synapse loss in IVD seems to be variable among IVD subtypes, probably reflecting its variable neuropathologic correlates. Loss of synaptic protein has been identified in vascular dementia of the Binswanger type and Spatz-Lindenberg's disease. Here we demonstrate a significant loss of synaptophysin density within the temporal lobe of frontotemporal dementia (FTD) patients.
突触传递对于神经系统功能至关重要，其功能障碍是导致阿尔茨海默病样痴呆的已知主要因素之一。抗原特异性免疫化学方法能够通过量化参与突触循环的各种突触蛋白来描述痴呆症中的突触损失。这些免疫化学方法应用于阿尔茨海默病 (AD) 脑标本的研究，已经将突触损失与特别有毒的淀粉样β蛋白形式相关联，并将突触损失确立为与痴呆严重程度的最佳相关性。大量但相对有限的文献描述了其他形式痴呆症中的突触衰退。缺血性血管性痴呆 (IVD) 非常多样化，IVD 中的突触损失似乎在 IVD 亚型之间存在差异，可能反映了其可变的神经病理学相关性。在宾斯旺格型血管性痴呆和斯帕茨-林登贝格病中已经发现了突触蛋白的丧失。在这里，我们在额颞叶痴呆 (FTD) 患者的颞叶中证明了突触素密度的显著丧失。
