Intranasal Aβ1−42 Exposure Led To Neurobehavioral Alteration, Neuroinflammatory and Neurodegenerative Molecular Biomarkers in Mice Brain
摘要
In this study, we aimed to evaluate the AD structural hallmarks along with brain biomarkers and neurobehavioral alterations in a repeated intranasal Aβ1−42 exposure mouse model. This model is a simple, non-invasive, and less stressful method and may allow direct access of Aβ to the brain. The results of this study showed a dose-dependent increase in the level of Aβ1−42 deposition, tau phosphorylation, neuroinflammatory and oxidative stress biomarkers in brain tissue, along with learning and memory deficits in mice. This model may be suitable for evaluating the biochemical, structural, functional histological alterations, along with the neurobehavioral deficits mimicking AD.
Graphical Abstract