INTRODUCTION
Inflammatory events significantly contribute to Alzheimer's disease pathogenesis. Growing evidence suggests midlife as a period of unique susceptibility to factors that can confer protection or susceptibility to later cognitive health or dementia. In humans, inflammation during midlife is associated with risk for cognitive decline and AD that emerge decades later. In addition, transient viral infections can lead to long lasting post-viral syndromes that emerge after a transient illness. Some viral illnesses (e.g., COVID-19, influenza, and shingles), are also associated with faster progression of AD and elevated AD risk later in life We have previously demonstrated that in young adult mice, short term / transient inflammation causes long lasting cognitive decline in both sexes and sex-specific changes in hippocampal gene expression (Tchessalova & Tronson 2019, 2020). Others have demonstrated that a single immune challenge via lipopolysaccharides injection accelerates progression of amyloid β (Aβ) and memory decline in transgenic AD mice. Here, new data demonstrates the impact of transient viral-like immune challenge in midlife (9-12 months) male and female mice on cognitive decline and AD progression.