• Carina Ledezma, Cinthia Coria-Lucero, María Belén Delsouc, Marilina Casais, Della Vedova Cecilia C Instituto de Química de San Luis (INQUISAL), CONICET, Ejército de Los Andes 950, CP D5700HHW San Luis, Argentina., Darío Ramirez, Cristina Mabel Devia, Silvia Marcela Delgado, Lorena Navigatore-Fonzo, and Ana Cecilia Anzulovich.
• Laboratorio de Cronobiología, Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis Instituto Multidisciplinario de Investigaciones Biológicas de San Luis (IMIBIO-SL), CONICET, Ejército de Los Andes 950, CP D5700HHW San Luis, Argentina.
• Neuroscience. 2021 Mar 15; 458: 99-107.

AbstractAccumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer's disease (AD). Aggregated beta-amyloid (Aβ) 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 Aβ (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 Aβ-injected (Aβ). 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 Aβ(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 Aβ 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.Copyright © 2020. Published by Elsevier Ltd.

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