by Laura O’Dea, Meredith LeBel, Nicole Haynes
Faculty mentor: Dr. Deborah O’Dell
Alzheimer’s disease (AD) is a neurodegenerative disease that affects more than 40 million people. While the pathophysiology has yet to be fully elucidated, some studies suggest AD associated chronic inflammation is caused by hyperactive microglia that produce pro-inflammatory factors. Probiotics have been shown to have anti-inflammatory properties and may influence neurochemistry via the gut-brain-axis, which controls communication between the intestines and brain, crossing over the blood brain barrier (BBB). A model of the BBB was constructed with a double transwell system to clarify the effects of probiotics on cerebral inflammation. Microglia cells grown in the basolateral chamber were co-cultured with endothelial cells in the upper compartment while an astrocyte monolayer separated the two compartments. Once the system was exposed to human peripheral blood T-cells and combined with histamine (probiotic anti-inflammatory product), formic acid (probiotic inflammatory product), both, or neither, the microglial medium was collected and analyzed for tumor necrosis factor α (TNFα) and interleukin-10 using ELISA. ANOVA and T-Tests were run and showed no significant results, except for the histamine and formic acid combination. In the combination treatment, levels of TNFα were slightly different than the control (p = 0.00006), contrary to what was expected. Under these conditions, probiotics do not reduce inflammation in the brain and thus cannot effectively treat AD patients. However, in the future, more experiments should be conducted with multiple inflammatory and anti-inflammatory molecules as there could be overlapping interactions between several probiotic products that produce advantageous metabolic effects and mitigate elevations in inflammatory responses.