Cannula Implantation Reduces the Severity of the Beta Amyloid Effect on Peroxidized Lipids and Glutathione Levels in the Brain of BALB/c Mice

Abstract

Sporadic Alzheimer’s disease (sAD) is the most common of neurodegenerative disorders. The lack of effective therapy indicates that the mechanisms of sAD development remain poorly understood. To investigate this pathology in animals, intracerebroventricular injection of β-amyloid peptide (Aβ) using a Hamilton syringe, either during stereotactic surgery or through a pre-implanted cannula, is used. In this study, we analyzed the effect of chronic cannula implantation on the severity of Aβ effects at the behavioral, histological, and biochemical levels. The results showed that the local damage to neural tissue caused by cannulation has no bearing on the effect of Aβ on animal behavior and the microglial parameters of the unilateral hippocampus two weeks after the Aβ administration. However, cannula implantation fundamentally modifies some biochemical markers of the oxidative stress that occurs in the brain tissue in response to Aβ administration. Thus, the presence of a cannula reduces the severity of the Aβ impact on the levels of peroxidized lipids and glutathione two- and 10-fold, respectively. It is important to note that the detected changes are chronic and systemic. This is known because the homogenate of the entire contralateral (in relation to the cannula implantation site) hemisphere was analyzed, and the analysis was performed two weeks after implantation. At the same time, cannulation does not affect the rate of reactive oxygen species production. The obtained data indicate that chronic implantation of a cannula into the brain of experimental animals fundamentally distorts some parameters of oxidative stress in the neural tissue, which are widely used to assess the severity of experimental Alzheimer’s-type diseases.