Mostrar el registro sencillo del ítem
Dexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways
dc.contributor.author | Ettcheto M. | |
dc.contributor.author | Sánchez-López E. | |
dc.contributor.author | Pons L. | |
dc.contributor.author | Busquets O. | |
dc.contributor.author | Olloquequi J. | |
dc.contributor.author | Beas-Zarate C. | |
dc.contributor.author | Pallas M. | |
dc.contributor.author | García M.L. | |
dc.contributor.author | Auladell C. | |
dc.contributor.author | Folch J. | |
dc.contributor.author | Camins A. | |
dc.date.accessioned | 2020-09-02T22:17:22Z | |
dc.date.available | 2020-09-02T22:17:22Z | |
dc.date.issued | 2017 | |
dc.identifier | 10.1016/j.redox.2017.06.003 | |
dc.identifier.citation | 13, , 345-352 | |
dc.identifier.issn | 22132317 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4412 | |
dc.description | The aim of the present study is to elucidate the neuronal pathways associated to NSAIDs causing a reduction of the risk and progression of Alzheimer's disease. The research was developed administering the active enantiomer of ibuprofen, dexibuprofen (DXI), in order to reduce associated gastric toxicity. DXI was administered from three to six-month-old female APPswe/PS1dE9 mice as a model of familial Alzheimer's disease. DXI treatment reduced the activation of glial cells and the cytokine release involved in the neurodegenerative process, especially TNFα. Moreover, DXI reduced soluble β-amyloid (Aβ1-42) plaque deposition by decreasing APP, BACE1 and facilitating Aβ degradation by enhancing insulin-degrading enzyme. DXI also decreased TAU hyperphosphorylation inhibiting c-Abl/CABLES/p-CDK5 activation signal pathway and prevented spatial learning and memory impairment in transgenic mice. Therefore, chronic DXI treatment could constitute a potential AD-modifying drug, both restoring cognitive functions and reversing multiple brain neuropathological hallmarks. © 2017 The Authors | |
dc.language.iso | en | |
dc.publisher | Elsevier B.V. | |
dc.subject | Alzheimer's disease | |
dc.subject | APPSwe/PS1dE9 | |
dc.subject | Dexibuprofen | |
dc.subject | Hippocampus | |
dc.subject | Insulin receptor | |
dc.subject | Memory impairment | |
dc.subject | Mitochondria | |
dc.subject | TAU | |
dc.subject | Abelson kinase | |
dc.subject | amyloid beta protein[1-42] | |
dc.subject | beta secretase 1 | |
dc.subject | cyclin dependent kinase 5 | |
dc.subject | dexibuprofen | |
dc.subject | tau protein | |
dc.subject | Abelson kinase | |
dc.subject | amyloid precursor protein | |
dc.subject | aspartic proteinase | |
dc.subject | Bace1 protein, mouse | |
dc.subject | Cables1 protein, mouse | |
dc.subject | carrier protein | |
dc.subject | Cdk5 protein, mouse | |
dc.subject | cyclin dependent kinase 5 | |
dc.subject | cycline | |
dc.subject | dexibuprofen | |
dc.subject | ibuprofen | |
dc.subject | neuroprotective agent | |
dc.subject | phosphoprotein | |
dc.subject | presenilin 1 | |
dc.subject | secretase | |
dc.subject | tau protein | |
dc.subject | tumor necrosis factor | |
dc.subject | Alzheimer disease | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | Article | |
dc.subject | cell activation | |
dc.subject | cognition assessment | |
dc.subject | controlled study | |
dc.subject | disease course | |
dc.subject | enzyme linked immunosorbent assay | |
dc.subject | female | |
dc.subject | glia cell | |
dc.subject | immunofluorescence | |
dc.subject | male | |
dc.subject | memory disorder | |
dc.subject | mental deterioration | |
dc.subject | mouse | |
dc.subject | nerve degeneration | |
dc.subject | nonhuman | |
dc.subject | priority journal | |
dc.subject | protein degradation | |
dc.subject | protein phosphorylation | |
dc.subject | real time polymerase chain reaction | |
dc.subject | signal transduction | |
dc.subject | spatial learning | |
dc.subject | treatment outcome | |
dc.subject | treatment response | |
dc.subject | Western blotting | |
dc.subject | Alzheimer disease | |
dc.subject | analogs and derivatives | |
dc.subject | animal | |
dc.subject | brain | |
dc.subject | C57BL mouse | |
dc.subject | cognition | |
dc.subject | drug effects | |
dc.subject | genetics | |
dc.subject | metabolism | |
dc.subject | signal transduction | |
dc.subject | Alzheimer Disease | |
dc.subject | Amyloid beta-Protein Precursor | |
dc.subject | Amyloid Precursor Protein Secretases | |
dc.subject | Animals | |
dc.subject | Aspartic Acid Endopeptidases | |
dc.subject | Brain | |
dc.subject | Carrier Proteins | |
dc.subject | Cognition | |
dc.subject | Cyclin-Dependent Kinase 5 | |
dc.subject | Cyclins | |
dc.subject | Female | |
dc.subject | Ibuprofen | |
dc.subject | Mice | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Neuroprotective Agents | |
dc.subject | Phosphoproteins | |
dc.subject | Presenilin-1 | |
dc.subject | Proto-Oncogene Proteins c-abl | |
dc.subject | Signal Transduction | |
dc.subject | tau Proteins | |
dc.subject | Tumor Necrosis Factor-alpha | |
dc.title | Dexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways | |
dc.type | Article |