Expression Profiling of Cytokine, Cholinergic Markers, and Amyloid-β Deposition in the APP SWE /PS1dE9 Mouse Model of Alzheimer's Disease Pathology

Background: Alzheimer's disease (AD), a neurodegenerative disease, is associated with dysfunction of the olfactory and the entorhinal cortex of the brain that control memory and cognitive functions and other daily activities. Pro-inflammatory cytokines, amyloid-β(Aβ), and the cholinergic system play vital roles in the pathophysiology of AD. However, the role of changes in cholinergic system components, Aβ accumulation, and cytokines in both the olfactory and entorhinal cortex is not known clearly. Objective: The present study is aimed to evaluate the changes of cholinergic system components, A accumulation, and cytokines in both the olfactory bulb (OB) and entorhinal cortex (EC) of young and aged APP SWE /PS1dE9 transgenic (Tg) mice. Methods: We have explored the changes of cholinergic system components, Aβ accumulation, and expression profiling of cytokines in the OB and EC of aged APPswe transgenic mice and age-matched wild type mice using quantitative Real-Time PCR assays and immunohistochemistry techniques. Results: In aged Tg mice, a significant increase of expression of interleukin (IL)-1β tumor necrosis factor (TNF)-α, and chemokine MCP1 (p < 0.001, p < 0.001, and p = 0.001, respectively) and a significant reduction of nAChRα4 (p = 0.048) and AChE (p = 0.023) was observed when compared with age-matched wild type mice. Higher levels of AChE and BuChE are expressed in OB and EC of the APP SWE /PS1dE9 of Tg mice. A accumulation was observed in OB and EC of the APP SWE /PS1dE9 of Tg mice. Conclusion: The study demonstrates the expression profiling of pro-inflammatory cytokines and cholinergic markers as well as A accumulation in OB and EC of the APP SWE /PS1dE9 Tg mice. Moreover, the study also demonstrated that the APP SWE /PS1dE9 Tg mice can be useful as a mouse model to understand the role of pro-inflammatory cytokines and cholinergic markers in pathophysiology of AD.