Newman Ehren L, Shay Christopher F, Hasselmo Michael E
Center for Memory & Brain, Boston University, 2 Cummington St, Boston, MA 02215, USA.
Future Neurol. 2012 Sep;7(5):557-571. doi: 10.2217/fnl.12.47.
In this article, we will describe the malignant synaptic growth hypothesis of Alzheimer's disease. Originally presented in 1994, the hypothesis remains a viable model of the functional and biophysical mechanisms underlying the development and progression of Alzheimer's disease. In this article, we will refresh the model with references to relevant empirical support that has been generated in the intervening two decades since it's original presentation. We will include discussion of its relationship, in terms of points of alignment and points of contention, to other models of Alzheimer's disease, including the cholinergic hypothesis and the tau and β-amyloid models of Alzheimer's disease. Finally, we propose several falsifiable predictions made by the malignant synaptic growth hypothesis and describe the avenues of treatment that hold the greatest promise under this hypothesis.
在本文中,我们将描述阿尔茨海默病的恶性突触生长假说。该假说最初于1994年提出,至今仍是阿尔茨海默病发生发展背后功能和生物物理机制的一个可行模型。在本文中,我们将参考自该假说首次提出后的二十年间所产生的相关实证支持来更新这个模型。我们将讨论它与其他阿尔茨海默病模型(包括胆碱能假说以及阿尔茨海默病的tau蛋白和β淀粉样蛋白模型)在一致性和争议点方面的关系。最后,我们提出恶性突触生长假说所做出的几个可证伪的预测,并描述在这一假说下最具前景的治疗途径。