A Bioinformatics Analysis of Gene Expression Changes in Human Alzheimer's Disease and Mouse Models

Abstract

Alzheimers disease (AD), the most common form of dementia, affects more than 50 million people worldwide, with no current treatment to halt the disease. The exact molecular mechanisms modulating disease progression remains elusive, even though numerous studies using mouse AD models have been done. In addition, as mouse models do not fully recapitulate human pathology, it is unclear to what extent results acquired from mouse models can be applied to treat humans. In this study, we conducted comprehensive bioinformatics analyses on transcriptomic profiles from mice bearing Abeta or tau pathology and human AD to identify differentially expressed genes (DEGs) and biological pathways shared among them. We identified the disease-associated microglia (DAM) signature and inflammatory pathways in both amyloid and tau mouse models compared to controls. Although GFAP was the only DEG shared by human AD and mouse AD models, pathways such as inflammatory response were identified in both human and mouse. Common pathways found in this study may modulate disease progression and provide new therapeutic targets.