Event Title

Sex-Specific Changes in Brain Amyloidosis and Microglia Phenotype in Germ-Free APPPS1-21 Alzheimer’s Transgenic Mice

Advisor(s)

Dr. Sangram Sisodia; University of Chicago

Discipline

Medical and Health Sciences

Start Date

21-4-2021 9:30 AM

End Date

21-4-2021 9:45 AM

Abstract

Recent evidence suggests that gut microbiota play a critical role in regulating innate immunity and influencing brain function. Clinical studies revealed an association between brain amyloidosis and the presence of pathogenic bacteria in the gut of cognitively impaired patients. Our previous study concluded that an ABX-perturbed microbiome has selective, sex-specific influences on brain amyloid (Abeta) amyloidosis and microglial homeostasis. The actual mechanism by which the gut microbiome influences Alzheimer's pathogenesis has yet to be identified. Here, we explored germfree (GF) Alzheimer's transgenic APPPS1-21 mice for amyloidosis and microgliosis phenotype. Both GF male and female mice showed significantly larger ceca compared with specific-pathogen free (SPF) mice. Cerebral amyloidosis was quantified using 3D6 marker and immunohistochemistry. Data from this study strengthen our previously established microbiota-brain axis results. Upcoming experiments exploring cortical transcriptome profiles will shed light on the neuro-immune interaction in this GF APPPS1-21 mouse model.

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Apr 21st, 9:30 AM Apr 21st, 9:45 AM

Sex-Specific Changes in Brain Amyloidosis and Microglia Phenotype in Germ-Free APPPS1-21 Alzheimer’s Transgenic Mice

Recent evidence suggests that gut microbiota play a critical role in regulating innate immunity and influencing brain function. Clinical studies revealed an association between brain amyloidosis and the presence of pathogenic bacteria in the gut of cognitively impaired patients. Our previous study concluded that an ABX-perturbed microbiome has selective, sex-specific influences on brain amyloid (Abeta) amyloidosis and microglial homeostasis. The actual mechanism by which the gut microbiome influences Alzheimer's pathogenesis has yet to be identified. Here, we explored germfree (GF) Alzheimer's transgenic APPPS1-21 mice for amyloidosis and microgliosis phenotype. Both GF male and female mice showed significantly larger ceca compared with specific-pathogen free (SPF) mice. Cerebral amyloidosis was quantified using 3D6 marker and immunohistochemistry. Data from this study strengthen our previously established microbiota-brain axis results. Upcoming experiments exploring cortical transcriptome profiles will shed light on the neuro-immune interaction in this GF APPPS1-21 mouse model.