ArticleFrontiers in aging neuroscience2018
The Role of Fluoxetine in Activating Wnt/β-Catenin Signaling and Repressing β-Amyloid Production in an Alzheimer Mouse Model.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Emerging Therapeutic Potential of Fluoxetine on Cognitive Decline in Alzheimer's Disease: Systematic Review.International journal of molecular sciences · 2024Pooled it
- Exercise and fluoxetine in Alzheimer's disease: Molecular mechanisms of synergistic and antagonistic effects (Review).International journal of molecular medicine · 2026Review
- Disodium cromoglycate restricts human tau hyperphosphorylation and manifestation of associated phenotypes by inhibiting GSK3β activity in Drosophila disease models.Molecular biology reports · 2026Article
- Fluoxetine Repurposing Mitigates Alzheimer's Disease Pathology via the GSK3β-CREB-ADAM10 Axis.International journal of molecular sciences · 2026Article
- Wnt/β-catenin Pathway Activation Reverses Tau Hyperphosphorylation and β-Amyloid Accumulation Induced by Combined Manganese and Iron Exposure in PC12 Cells.Biological trace element research · 2026Article
- The Synergistic Role of ApoE4 and GSK3β in Alzheimer's Disease: Pathological Mechanisms and Therapeutic Implications.Molecular neurobiology · 2025Review
- Prioritizing repurposable drugs for Alzheimer's disease using network-based analysis with concurrent assessment of Long QT syndrome risk.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- Immunopsychiatry of late life depression: role of ageing-related immune/inflammatory processes in the development and progression of depression.Acta neuropsychiatrica · 2025Review
- Unlocking Hope: Therapeutic Advances and Approaches in Modulating the Wnt Pathway for Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Drugs repurposing in the experimental models of Alzheimer's disease.Inflammopharmacology · 2025Review
- Exploring the Complex Relationship Between Antidepressants, Depression and Neurocognitive Disorders.Biomedicines · 2024Review
- Systemic Modulators: Potential Mechanism for the 5-HT System to Mediate Exercise Amelioration in Alzheimer's Disease.Aging and disease · 2024Review
- Fluoxetine Rescues Excessive Myelin Formation and Psychological Behaviors in a Murine PTSD Model.Neuroscience bulletin · 2024Article
- GSK3: A potential target and pending issues for treatment of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Special Issue "Pathophysiology and Treatment of Alzheimer's Disease".International journal of molecular sciences · 2024Article
- Converged avenues: depression and Alzheimer's disease- shared pathophysiology and novel therapeutics.Molecular biology reports · 2024Review
- Therapeutic potential of melatonin and its derivatives in aging and neurodegenerative diseases.Biogerontology · 2023Review
- From attention-deficit hyperactivity disorder to sporadic Alzheimer's disease-Wnt/mTOR pathways hypothesis.Frontiers in neuroscience · 2023Article
- Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2023Review
- Boosting Neurogenesis in the Adult Hippocampus Using Antidepressants and Mesenchymal Stem Cells.Cells · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fluoxetine (FLX) is one of the selective serotonin reuptake inhibitors (SSRIs) antidepressants, which could be used to relieve depression and anxiety among AD patients. This study was designed to search for new mechanisms by which fluoxetine could activate Wnt/β-catenin signaling pathway and reduce amyloidosis in AD brain. Fluoxetine was administered via intragastric injection to APP/tau/PS1 mouse model of Alzheimer's disease (3×Tg-AD) mice for 4 months. In the hippocampus of AD mouse model, there could be observed neuronal apoptosis, as well as an increase in Aβ (amyloid-β) production. Moreover, there is a strong association between down-regulation of Wnt/β-catenin signaling and the alteration of AD pathology. The activity of protein phosphatases of type 2A (PP2A) could be significantly enhanced by the treatment of fluoxetine. The activation of PP2A, caused by fluoxetine, could then play a positive role in raising the level of active β-catenin, and deliver a negative impact in GSK3β activity in the hippocampal tissue. Both the changes mentioned above would lead to the activation of Wnt/β-catenin signaling. Meanwhile, fluoxetine treatment would reduce APP cleavage and Aβ generation. It could also prevent apoptosis in 3×Tg-AD primary neuronal cell, and have protective effects on neuron synapse. These findings imply that Wnt/β-catenin signaling could be a potential target outcome for AD prevention, and fluoxetine has the potential to be a promising drug in both AD prevention and treatment.
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