2026-04-13T07:14:30Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1188472025-11-19T10:41:59Zcom_2072_1057col_2072_478777col_2072_478815col_2072_478816col_2072_478917

00925njm 22002777a 4500 dc Ettcheto Arriola, Miren author Sánchez-López, E. (Elena) author Pons, Laura author Busquets Figueras, Oriol author Olloquequi, Jordi author Beas Zárate, Carlos author Pallàs i Llibería, Mercè, 1964- author García López, María Luisa author Auladell i Costa, M. Carme author Folch, Jaume author Camins Espuny, Antoni author 2017-12-21T14:20:21Z 2017-12-21T14:20:21Z 2017-06-15 2017-12-21T14:20:21Z 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. Malaltia d'Alzheimer Hipocamp (Cervell) Receptors d'insulina Mitocondris Medicaments Alzheimer's disease Hippocampus (Brain) Insulin receptors Mitochondria Drugs Dexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways.