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Abstract：
Alzheimer\'s disease (AD) is a neurodegenerative disease and the most common example of dementia. The neuropathological features of AD are the abnormal deposition of extracellular amyloid-β (Aβ) and intraneuronal neurofibrillary tangles with hyperphosphorylated tau protein. It is recognized that AD starts in the frontal cerebral cortex, and then it progresses to the entorhinal cortex, the hippocampus, and the rest of the brain. However, some studies on animals suggest that AD could also progress in the reverse order starting from the midbrain and then spreading to the frontal cortex. Spirochetes are neurotrophic: From a peripheral route of infection, they can reach the brain via the midbrain. Their direct and indirect effect via the interaction of their virulence factors and the microglia potentially leads to the host peripheral nerve, the midbrain (especially the locus coeruleus), and cortical damage. On this basis, this review aims to discuss the hypothesis of the ability of Treponema denticola to damage the peripheral axons in the periodontal ligament, to evade the complemental pathway and microglial immune response, to determine the cytoskeletal impairment and therefore causing the axonal transport disruption, an altered mitochondrial migration and the consequent neuronal apoptosis. Further insights about the central neurodegeneration mechanism and Treponema denticola\'s resistance to the immune response when aggregated in biofilm and its quorum sensing are suggested as a pathogenetic model for the advanced stages of AD.
摘要：
阿尔茨海默病（AD）是一种神经退行性疾病，也是最常见的痴呆症。AD的神经病理学特征是细胞外淀粉样β（Aβ）的异常沉积和神经元内神经原纤维缠结与高磷酸化tau蛋白。人们认识到AD开始于额叶大脑皮层,然后进展到内嗅皮层，海马体,和大脑的其余部分。然而,一些对动物的研究表明，AD也可能以相反的顺序从中脑开始，然后扩散到额叶皮层。螺旋体是神经营养性的：从外周感染途径，它们可以通过中脑到达大脑。它们的直接和间接作用通过它们的毒力因子和小胶质细胞的相互作用潜在地导致宿主周围神经,中脑（尤其是蓝斑），和皮质损伤。在此基础上,本文旨在探讨树突状螺旋体损伤牙周膜外周轴突的假说,逃避互补途径和小胶质细胞免疫反应，确定细胞骨架损伤，从而导致轴突运输中断，改变的线粒体迁移和随之而来的神经元凋亡。关于中枢神经变性机制和树突状螺旋体在生物膜中聚集时对免疫反应的抗性及其群体感应的进一步见解被认为是AD晚期的致病模型。
