Accelerating neuronal aging in in vitro model brain disorders: a focus on reactive oxygen species

被引:44
作者
Campos, Priscila Britto [1 ]
Paulsen, Bruna S. [1 ]
Rehen, Stevens K. [1 ,2 ]
机构
[1] Univ Fed Rio de Janeiro, Inst Biomed Sci, Rio De Janeiro, Brazil
[2] DOr Inst Res & Educ IDOR, BR-22281100 Rio De Janeiro, Brazil
关键词
Parkinson; Alzheimer; schizophrenia; aged neurons; ROS; pluripotent stem cells; MITOCHONDRIAL COMPLEX-I; PLURIPOTENT STEM-CELLS; OXIDATIVE STRESS; NEURODEGENERATIVE DISEASES; PARKINSONS-DISEASE; SCHIZOPHRENIA; ADENOSINE; INFLAMMATION; HYPERPHOSPHORYLATION; DIFFERENTIATION;
D O I
10.3389/fnagi.2014.00292
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
030301 [社会学]; 100201 [内科学];
摘要
In this review, we discuss insights gained through the use of stem cell preparations regarding the modeling of neurological diseases, the need for aging neurons derived from pluripotent stem cells to further advance the study of late-onset adult neurological diseases, and the extent to which mechanisms linked to the mismanagement of reactive oxygen species (ROS). The context of these issues can be revealed using the three disease states of Parkinson's (PD), Alzheimer's (AD), and schizophrenia, as considerable insights have been gained into these conditions through the use of stem cells in terms of disease etiologies and the role of oxidative stress. The latter subject is a primary area of interest of our group. After discussing the molecular models of accelerated aging, we highlight the role of ROS for the three diseases explored here. Importantly, we do not seek to provide an extensive account of all genetic mutations for each of the three disorders discussed in this review, but we aim instead to provide a conceptual framework that could maximize the gains from merging the approaches of stem cell microsystems and the study of oxidative stress in disease in order to optimize therapeutics and determine new molecular targets against oxidative stress that spare stem cell proliferation and development.
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页数:10
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