Currais Antonio, Hortobágyi Tibor, Soriano Salvador
Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College London, London SE5 8AF, UK.
Aging (Albany NY). 2009 Apr 28;1(4):363-71. doi: 10.18632/aging.100045.
Differentiated neurons display specific biochemical, physiological and morphological properties that apparently prevent them from further cell division. Nevertheless, expression of cell cycle modulators persists after neuronal differentiation and is upregulated under stress conditions, such as trophic factor deprivation, oxidative stress and the presence of DNA damaging agents. This apparent reactivation of the cell cycle has been postulated as a sine qua non for neuronal death in response to those stress conditions, particularly in Alzheimer's disease. However, the physiological and pathogenic implications of a putative neuronal cell cycle are far from clear. Here, we discuss the notion of the neuronal cell cycle as a mediator of cell death, with particular emphasis on Alzheimer's disease.
分化的神经元表现出特定的生化、生理和形态学特性,这些特性显然使其无法进一步进行细胞分裂。然而,细胞周期调节因子在神经元分化后仍持续表达,并在应激条件下上调,如营养因子剥夺、氧化应激和DNA损伤剂的存在。这种细胞周期的明显重新激活被认为是这些应激条件下神经元死亡的必要条件,特别是在阿尔茨海默病中。然而,假定的神经元细胞周期的生理和致病意义尚不清楚。在这里,我们讨论神经元细胞周期作为细胞死亡介质的概念,特别强调阿尔茨海默病。