Prenatal stress increases the risk of the FPR2-related dysfunction in the brain's resolution of inflammation: a study on the humanized APPNL-F/NL-F mouse model of Alzheimer's disease

Chronic neuroinflammation and impaired resolution of inflammation (RoI) are critical contributors to the development of Alzheimer’s disease and related cognitive decline. Prenatal stress (PS) is an important environmental factor that may disrupt these processes and promote long-term alterations in brain function. Formyl peptide receptor 2 (FPR2) plays a central role in regulating pro-resolving pathways in the brain.The aim of the study was to investigate the age-dependent effects of prenatal stress on cognitive function, neuroinflammation, and FPR2-related resolution pathways in the hippocampus and frontal cortex of wild-type and APPNL-F/NL-F (KI) mice.The dataset includes experimental data corresponding to all figures and tables presented in the publication. It comprises behavioral data from cognitive and locomotor tests (Morris Water Maze, Open Field), as well as biochemical and molecular analyses. These include measurements of amyloid pathology (Aβ42/Aβ40 ratio), expression of FPR2 and its pro-resolving ligands (LXA4, ANXA1), and markers of microglial phenotype (iNos, Cd40, Ym1, Arg1). Additionally, the dataset contains senescence markers (p53, p16, pRb), cytokine levels (IL-1β, IL-10, TGF-β), and key signaling pathway components, including NF-κB activation, A20 (TNFAIP3), and NLRP3 inflammasome proteins (NLRP3, caspase-1, ASC).Our results identify the FPR2 receptors as a driver regulating the RoI process in the brain and highlight that PS has diversified the picture of age-dependent neurodegenerative pathology.