ArticleMolecular neurobiology2019
Reboxetine Treatment Reduces Neuroinflammation and Neurodegeneration in the 5xFAD Mouse Model of Alzheimer's Disease: Role of CCL2.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Reboxetine Treatment Reduces Hippocampal Gliosis in the P301S Tauopathy Mouse Model.ASN neuro · 2026Article
- Bridging the barrier: insights into blood biomarkers and therapeutic strategies targeting choroid plexus and BBB dysfunction in alzheimer's disease.Biomarker research · 2025Review
- Regenerating Locus Coeruleus-Norepinephrine (LC-NE) Function: A Novel Approach for Neurodegenerative Diseases.Cell proliferation · 2025Review
- Monoamine alterations in Alzheimer's disease and their implications in comorbid neuropsychiatric symptoms.GeroScience · 2025Review
- Infections withFrontiers in aging neuroscience · 2025Review
- Psilocin, the Psychoactive Metabolite of Psilocybin, Modulates Select Neuroimmune Functions of Microglial Cells in a 5-HTMolecules (Basel, Switzerland) · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- P2XBrain, behavior, and immunity · 2023Article
- Dietary Polyphenols Decrease Chemokine Release by Human Primary Astrocytes Responding to Pro-Inflammatory Cytokines.Pharmaceutics · 2023Article
- Role of Chemokines in the Development and Progression of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Review
- Analysis of transcriptome characteristics of UTI therapy for cerebral injury after CA/ROSC based on RNA-seq technique.Iranian journal of basic medical sciences · 2022Article
- Noradrenaline in Alzheimer's Disease: A New Potential Therapeutic Target.International journal of molecular sciences · 2022Review
- CCL2 Inhibition of Pro-Resolving Mediators Potentiates Neuroinflammation in Astrocytes.International journal of molecular sciences · 2022Article
- Targeting the CCL2-CCR2 axis in depressive disorders.Pharmacological reports : PR · 2021Review
- Glucagon-like peptide-1 analog improves neuronal and behavioral impairment and promotes neuroprotection in a rat model of aluminum-induced dementia.Physiological reports · 2021Article
- Mesenchymal stem cell-derived extracellular vesicles ameliorate Alzheimer's disease-like phenotypes in a preclinical mouse model.Theranostics · 2021Article
- Locus Coeruleus Modulates Neuroinflammation in Parkinsonism and Dementia.International journal of molecular sciences · 2020Review
- Dietary Wheat Amylase Trypsin Inhibitors Impact Alzheimer's Disease Pathology in 5xFAD Model Mice.International journal of molecular sciences · 2020Article
- Early intraneuronal amyloid triggers neuron-derived inflammatory signaling in APP transgenic rats and human brain.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The reduction of brain noradrenaline levels is associated to the initiation of Alzheimer's disease and contributes to its progression. This seems to be due mainly to the anti-neuroinflammatory actions of noradrenaline. The analysis of noradrenaline effects on brain cells demonstrates that it also regulates the production of the chemokine CCL2. In the present study, we analyzed the effect of the selective noradrenaline reuptake inhibitor, reboxetine, on the inflammatory and neurodegenerative alterations present in 5xFAD mice, and how the genetic removal of CCL2 affects reboxetine actions. We observed that the removal of CCL2 reduced the memory impairments in 5xFAD mice as well as the neuroinflammatory response, the accumulation of amyloid beta plaques, and the degeneration of neurons in the brain cortex. The administration of reboxetine with osmotic pumps for 28 days also resulted in anti-inflammatory and neuroprotective changes in 5xFAD mice, even in the absence of CCL2. Yet, 6-month-old CCL2KO mice presented a significant degree of neuroinflammation and neuronal damage. These findings indicate that reboxetine treatment prevents the brain alterations caused by prolonged overproduction of amyloid beta, being these effects independent of CCL2, which is a mediator of the damage caused by amyloid beta in the brain cortex, but necessary for the prevention of the development of neurodegeneration in normal healthy conditions.
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Registered trials
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