Department of Blood Transfusion, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Department of Pathology, Central Hospital of Wuhan, Wuhan, 430014, People's Republic of China.
Mol Neurobiol. 2018 Apr;55(4):3021-3032. doi: 10.1007/s12035-017-0533-3. Epub 2017 Apr 29.
Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory. However, the mechanism underlying these symptoms remains unclear. The best correlation between cognitive decline and pathological changes is in synaptic dysfunction. Histopathological hallmarks of AD are the abnormal aggregation of Aβ and Tau. Evidence suggests that Aβ and Tau oligomers contribute to synaptic loss in AD. Recently, direct links between epigenetic alterations, such as dysfunction in non-coding RNAs (ncRNAs), and synaptic pathologies have emerged, raising interest in exploring the potential roles of ncRNAs in the synaptic deficits in AD. In this paper, we summarize the potential roles of Aβ, Tau, and epigenetic alterations (especially by ncRNAs) in the synaptic dysfunction of AD and discuss the novel findings in this area.
阿尔茨海默病（AD）是一种复杂的神经退行性疾病，其早期特征是学习和记忆丧失。然而，这些症状的机制尚不清楚。认知能力下降与病理变化之间的最佳相关性在于突触功能障碍。AD 的组织病理学特征是 Aβ和 Tau 的异常聚集。有证据表明，Aβ和 Tau 寡聚物导致 AD 中的突触丧失。最近，表观遗传改变（如非编码 RNA（ncRNA）功能障碍）与突触病理之间的直接联系已经出现，这引起了人们对探索 ncRNA 在 AD 突触缺陷中的潜在作用的兴趣。在本文中，我们总结了 Aβ、Tau 和表观遗传改变（特别是 ncRNA）在 AD 突触功能障碍中的潜在作用，并讨论了该领域的新发现。
