ArticleRedox biology2017
Dexibuprofen prevents neurodegeneration and cognitive decline in APPswe/PS1dE9 through multiple signaling pathways.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- Exploring the role of COX-2 in Alzheimer's disease: Potential therapeutic implications of COX-2 inhibitors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Review
- Review
- Symptomatic and Disease-Modifying Therapy Pipeline for Alzheimer's Disease: Towards a Personalized Polypharmacology Patient-Centered Approach.International journal of molecular sciences · 2022Review
- JNK1 and JNK3: divergent functions in hippocampal metabolic-cognitive function.Molecular medicine (Cambridge, Mass.) · 2022Article
- Swimming training and Plantago psyllium ameliorate cognitive impairment and glucose tolerance in streptozotocin-nicotinamide-induced type 2 diabetic rats.The journal of physiological sciences : JPS · 2021Article
- Dexibuprofen ameliorates peripheral and central risk factors associated with Alzheimer's disease in metabolically stressed APPswe/PS1dE9 mice.Cell & bioscience · 2021Article
- Therapeutic Mechanism and Key Alkaloids ofFrontiers in pharmacology · 2021Article
- Epigallocatechin-3-Gallate (EGCG) Improves Cognitive Deficits Aggravated by an Obesogenic Diet Through Modulation of Unfolded Protein Response in APPswe/PS1dE9 Mice.Molecular neurobiology · 2020Article
- Article
- Microglial Hyperreactivity Evolved to Immunosuppression in the Hippocampus of a Mouse Model of Accelerated Aging and Alzheimer's Disease Traits.Frontiers in aging neuroscience · 2020Article
- Potential preventive disease-modifying pharmacological strategies to delay late onset Alzheimer's disease.Neural regeneration research · 2019Article
- Dual-drug loaded nanoparticles of Epigallocatechin-3-gallate (EGCG)/Ascorbic acid enhance therapeutic efficacy of EGCG in a APPswe/PS1dE9 Alzheimer's disease mice model.Journal of controlled release : official journal of the Controlled Release Society · 2019Article
- Exploring the Correlation between the Cognitive Benefits of Drug Combinations in a Clinical Database and the Efficacies of the Same Drug Combinations Predicted from a Computational Model.Journal of Alzheimer's disease : JAD · 2019Article
- A small diversity library of α-methyl amide analogs of sulindac for probing anticancer structure-activity relationships.Bioorganic & medicinal chemistry letters · 2018Article
- Royal Jelly Attenuates LPS-Induced Inflammation in BV-2 Microglial Cells through Modulating NF-Mediators of inflammation · 2018Article
- Dissecting the Potential Roles ofFrontiers in aging neuroscience · 2018Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.