| Autor: |
Puris E; School of Pharmacy, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland. elena.puris@uni-heidelberg.de.; Institute of Pharmacy and Molecular Biotechnology, Ruprecht-Karls-University, Im Neuenheimer Feld 329, 69120, Heidelberg, Germany. elena.puris@uni-heidelberg.de., Kouřil Š; Institute of Molecular and Translational Medicine, Palacký University Olomouc, Hněvotínská 5, 77900, Olomouc, Czech Republic.; Department of Clinical Biochemistry, University Hospital Olomouc, I.P. Pavlova 6, 77900, Olomouc, Czech Republic., Najdekr L; Institute of Molecular and Translational Medicine, Palacký University Olomouc, Hněvotínská 5, 77900, Olomouc, Czech Republic., Loppi S; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland.; Department of Immunobiology, University of Arizona, 1656 E Mabel Street, Tucson, AZ, 85724-5221, USA., Korhonen P; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland., Kanninen KM; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland., Malm T; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland., Koistinaho J; A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland.; Neuroscience Center, Helsinki Institute for Life Science, University of Helsinki, Haartmaninkatu 8, 00290, Helsinki, Finland., Friedecký D; Institute of Molecular and Translational Medicine, Palacký University Olomouc, Hněvotínská 5, 77900, Olomouc, Czech Republic.; Department of Clinical Biochemistry, University Hospital Olomouc, I.P. Pavlova 6, 77900, Olomouc, Czech Republic., Gynther M; School of Pharmacy, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland. |
| Abstrakt: |
Peripheral infections followed by systemic inflammation may contribute to the onset of Alzheimer`s disease (AD) and accelerate the disease progression later in life. Yet, the impact of systemic inflammation on the plasma and brain tissue metabolome and lipidome in AD has not been investigated. In this study, targeted metabolomic and untargeted lipidomic profiling experiments were performed on the plasma, cortices, and hippocampi of wild-type (WT) mice and transgenic APdE9 mice after chronic lipopolysaccharide (LPS) treatment, as well as saline-treated APdE9 mice. The lipidome and the metabolome of these mice were compared to saline-treated WT animals. In the brain tissue of all three models, the lipidome was more influenced than the metabolome. The LPS-treated APdE9 mice had the highest number of changes in brain metabolic pathways with significant alterations in levels of lysine, myo-inositol, spermine, phosphocreatine, acylcarnitines and diacylglycerols, which were not observed in the saline-treated APdE9 mice. In the WT mice, the effect of the LPS administration on metabolome and lipidome was negligible. The study provided exciting information about the biochemical perturbations due to LPS-induced inflammation in the transgenic AD model, which can significantly enhance our understanding of the role of systemic inflammation in AD pathogenesis. |
