Aberrant Neuronal Activity and Dysfunctional Connectivity in Aβ1–42- mediated Memory Deficits in Rats

Alzheimer's disease (AD) is a neurodegenerative disorder that gradually induces cognitive deficit. Working memory deficits have been previously reported in AD and Amyloid-β peptide (Aβ) is regarded as a causative factor for the impairments. Accumulating evidence has identified that neuronal ensemble activity as well as functional connectivity among neurons encode and process information in normal brain. How Aβ contributes to the abnormal neuronal ensemble activity and corresponding functional connectivity which, in turn, leads to the cognitive deficits? To address the issue, we simultaneously recorded neuronal activity from medial prefrontal cortex of rats (control and Aβ injected group) when the rats performed a Y-maze working memory task, to investigate the properties of neuronal ensemble activity and functional connectivity. In the control group, a group of neurons were collectively activated and the connectivity among the neurons strengthened during the working memory task. However, in the Aβ group, the neuronal activity and connectivity never experience significant change. Our results indicate that the dysfunction of neuronal activity and connectivity may provide insight for the Aβ-induced working memory deficits.