期刊
NEUROSCIENCE
卷 458, 期 -, 页码 99-107出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2020.08.016
关键词
Alzheimer's disease; beta amyloide peptide; experimental model; prefrontal cortex; circadian rhythms; redox change
资金
- National Agency for Promotion of Science and Technology (ANPCyT, Argentina) [PICT 2016-0332]
- National Council for Science and Technology (CONICET, Argentina) [PIP 0446]
- National University of San Luis (UNSL, Argentina) [PROICO 2-0518]
Injection of Aβ (1-42) in rat prefrontal cortex led to increased oxidative stress, decreased antioxidant defense, altered cellular redox state patterns, and potential contribution to Alzheimer's disease pathogenesis.
Accumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer's disease (AD). Aggregated beta-amyloid (A beta) peptide increases intracellular reactive oxygen species associated to a deficient antioxidant defense system. Prefrontal cortex plays a key role in memory and learning and is especially susceptible to oxidative stress. The objective of this work was to investigate the effects of an intracerebroventricular (i.c.v.) injection of A beta (1-42) on 24 h patterns of oxidative stress parameters and antioxidant defenses in the rat prefrontal cortex. Four-month-old male Holtzman rats were divided into two groups defined as: control (CO) and A beta-injected (A beta). Rats were maintained under12 h-light:12 h-dark conditions and received water and food ad libitum. Tissues samples were isolated every 6 h during a 24 h period. Interestingly, we found that an i.c.v. injection of A beta(1-42) increased lipid peroxidation, reduced total antioxidant capacity level, phase-shifted the daily peak of reduced glutathione, and had a differential effect on the oscillating catalase and glutathione peroxidase specific activity. Thus, elevated levels of A beta aggregates-a pathogenic hallmark of AD, caused altered temporal patterns of the cellular redox state in prefrontal cortex rat. These findings might contribute, at least in part, to the understanding of the molecular and biochemical basis of redox changes caused by circadian rhythms alterations observed in AD patients. (C) 2020 Published by Elsevier Ltd on behalf of IBRO.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据