Top correlates in each LV1 identified chemokines (MCP-1 in APP/PS1-STZ, MIP-1α and MIP-1β in APP/PS1xdb/db, MIP-1α in APP/PS1-HFD) that were only significantly upregulated in the presence of combined pathology (Figs. 1, 2, and 3, Additional file 1: Figures S3, S5, S7), emphasizing that the combined presence of amyloid and metabolic pathologies cooperatively modulates the neuroinflammatory environment. This evidence concerns the gene CCL3 and amyloidosis.