In neurodegenerative diseases such as Alzheimer's disease (AD), the appearance and accumulation of aggregates of Amyloid beta (Aβ) and phosphorylated Tau is triggered by some stimulus such as an immune response. Inflammatory bowel disease was also reported to be a risk factor for dementia in humans, but the mechanism remains unclear. The aim of this study is to develop novel therapeutic strategies by clarifying the immune responses that regulate the expansion of cells expressing Aβ and phosphorylated Tau.
We found that colitis enhanced the pathogenesis of AD, and immune cells were infiltrated in the brains and dura maters of mice models of AD by using scRNAseq, suggesting the involvement of immune responses in the development of neurological diseases.