The goal of this study is to investigate the involvement of inflammation in Alzheimers disease (AD) and to clarify the signaling pathways involved in the presence of beta-amyloidosis, a hallmark of AD pathogenesis, to help identifying potential targets for therapy. To do that, we isolated bone marrow-derived progenitor cells from femurs, tibiae and hip bones of non-transgenic C57BL/6 mice according to established protocols , and we maturated them with LPS. To obtain an unbiased view of gene regulation in mouse bone marrow-derived dendritic cells (BM-DCs) exposed to pre-aggregated beta-amyloid peptide (A) oligomers, we analyzed the transcriptome of untreated immature control BM-DCs (Ctrl), LPS-treated BM-DCs (LPS), A1-42 oligomer-treated BM-DCs (A) and BM-DCs treated with A1-42 oligomers and LPS (A+LPS) via explorative RNA-sequencing. SOURCE: Anna Mallone (anna.mallone@uzh.ch) -  University of Zurich

Pluto Bioinformatics

GSE136789: Oligomeric human A1-42 inhibits antigen presentation