阿尔茨海默病中的黏连与非整倍体表型：一个关于基因组不稳定的故事。

Cohesion and the aneuploid phenotype in Alzheimer's disease: A tale of genome instability.

作者信息

Bajic Vladan, Spremo-Potparevic Biljana, Zivkovic Lada, Isenovic Esma R, Arendt Thomas

机构信息

Institute for Nuclear Research "Vinca", Laboratory for Radiobiology and Molecular Genetics, University of Belgrade, P.O. 522, 11001 Belgrade, Serbia.

Faculty of Pharmacy, Institute of Physiology, Department of Biology and Human Genetics, University of Belgrade, Vojvode Stepe 450, 11000 Belgrade, Serbia.

出版信息

Neurosci Biobehav Rev. 2015 Aug;55:365-74. doi: 10.1016/j.neubiorev.2015.05.010. Epub 2015 May 21.

DOI:10.1016/j.neubiorev.2015.05.010

PMID:26003528

Abstract

Neurons are postmitotic cells that are in permanent cell cycle arrest. However, components of the cell cycle machinery that are expressed in Alzheimer's disease (AD) neurons are showing features of a cycling cell and those attributed to a postmitotic cell as well. Furthermore, the unique physiological operations taking place in neurons, ascribed to "core cell cycle regulators" are also key regulators in cell division. Functions of these cell cycle regulators include neuronal migration, axonal elongation, axon pruning, dendrite morphogenesis and synaptic maturation and plasticity. In this review, we focus on cohesion and cohesion related proteins in reference to their neuronal functions and how impaired centromere/cohesion dynamics may connect cell cycle dysfunction to aneuploidy in AD.

摘要

神经元是处于永久细胞周期停滞状态的有丝分裂后细胞。然而，在阿尔茨海默病（AD）神经元中表达的细胞周期机制成分既呈现出循环细胞的特征，也具有有丝分裂后细胞的特征。此外，神经元中发生的独特生理过程，归因于“核心细胞周期调节因子”，它们也是细胞分裂中的关键调节因子。这些细胞周期调节因子的功能包括神经元迁移、轴突伸长、轴突修剪、树突形态发生以及突触成熟和可塑性。在本综述中，我们聚焦于黏连蛋白和与黏连相关的蛋白质，涉及其神经元功能，以及着丝粒/黏连动力学受损如何将细胞周期功能障碍与AD中的非整倍体联系起来。