Cellular Redox Imbalance and Neurochemical Effect in Cognitive-Deficient Old Rats

Abstract

The purpose of the present study is to access the linkage between dysregulation of glutamatergic neurotransmission, oxidative metabolism, and serine signaling in age-related cognitive decline. In this work, we evaluated the effect of natural aging in rats on the cognitive abilities for hippocampal-dependent tasks. Oxidative metabolism indicators are glutathione (GSH), malondialdehyde (MDA) concentrations, and cytosolic phospholipase A2 (PLA2) activity. In addition, neurotransmitter amino acid (L-Glutamic acid, γ-aminobutyric acid (GABA), DL-Serine and DL-Aspartic acid) concentrations were studied in brain areas such as the frontal cortex (FC) and hippocampus (HPC). The spatial long-term memory revealed significant differences among experimental groups: the aged rats showed an increase in escape latency to the platform associated with a reduction of crossings and spent less time on the target quadrant than young rats. Glutathione levels decreased for analyzed brain areas linked with a significant increase in MDA concentrations and PLA2 activity in cognitive-deficient old rats. We found glutamate levels only increased in the HPC, whereas a reduced level of serine was found in both regions of interest in cognitive-deficient old rats. We demonstrated that age-related changes in redox metabolism contributed with alterations in synaptic signaling and cognitive impairment.

Estimated Phytate Intake Is Associated with Improved Cognitive Function in the Elderly, NHANES 2013–2014

“…MDA is a by-product of oxidative stress, lipid peroxidation and cell membrane damage [16]. Increased MDA may be observed in brain regions of Alzheimer's disease patients and in aged rats showing cognitive deficits [17,18]. In MC65 human neuroblastoma cells, 100 µM phytic acid in the presence of tetracycline resulted in reduced concentrations of hydrogen peroxide and increased concentrations of proteins responsible for autophagy and housekeeping of the neuroblastoma cells (beclin-1 and SIRT1) [12].…”