Posterior parietal cortex oscillatory activity shapes persistent spatial memory impairments induced by soluble amyloid-β oligomers

Abstract

Abstract Background: In early stages of Alzheimer's disease (AD), soluble amyloid-β (Aβ) is a key player disrupting neuronal activity and contributing to cognitive decline in advanced stages of the disease. While the hippocampus has been a central focus in prior research due to its susceptibility to Aβ-induced alterations, a comprehensive understanding of early AD pathology requires exploring interconnected brain regions. The posterior parietal cortex (PPC), collaborating closely with the hippocampus and involved in various memory processes, particularly spatial memory formation, holds particular significance. Investigating the PPC's function is imperative, as it may contribute to early AD characteristics and provide a more holistic perspective on disease progression. Methods: To address this gap, we examined the relationship between neural oscillations and memory processes in the PPC and hippocampus in a mouse model of early hippocampal amyloidosis generated by intracerebroventricular oligomeric Aβ1-42 (oAβ1‑42) injections by performing in vivo oscillatory activity recordings from these regions in alert animals, together with spatial and habituation memory tests (Barnes maze and open field habituation). Results: We found oAβ1-42 to induce significant alterations in PPC oscillatory activity emerging several days after hippocampal disturbances showed by aberrant long-term potentiation (LTP) and network activity. Additionally, non-significant alterations of stereotyped behaviors were found. Conclusions: Our results indicate that these atypical patterns provide insight into the persistent spatial memory deficits observed in our amyloidosis model and the temporal progression of the deleterious effects caused by Aβ. Furthermore, they support the potential use of PPC oscillatory activity as a valuable tool for early detection and intervention in AD.