ArticleNeuropharmacology
Fluoxetine protects against amyloid-beta toxicity, in part via daf-16 mediated cell signaling pathway, in Caenorhabditis elegans.
Article in Neuropharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Emerging Therapeutic Potential of Fluoxetine on Cognitive Decline in Alzheimer's Disease: Systematic Review.International journal of molecular sciences · 2024Pooled it
- The amino acid substitutions A30W, K28A, and M35C alter amyloid-β peptide toxicity in cell culture and in anFrontiers in aging neuroscience · 2026Article
- Systemic Modulators: Potential Mechanism for the 5-HT System to Mediate Exercise Amelioration in Alzheimer's Disease.Aging and disease · 2024Review
- Components in SLPE Alleviate AD Model Nematodes by Up-Regulating GeneInternational journal of molecular sciences · 2024Article
- Regulation of the proteostasis network by the neuronal system.Frontiers in molecular biosciences · 2023Review
- Anti-Oxidant and Anti-Aging Effects of Phlorizin Are Mediated by DAF-16-Induced Stress Response and Autophagy inAntioxidants (Basel, Switzerland) · 2022Article
- UsingFrontiers in pharmacology · 2022Review
- Sirtuins and Autophagy in Age-Associated Neurodegenerative Diseases: Lessons from theInternational journal of molecular sciences · 2021Review
- Can Animal Models Inform on the Relationship between Depression and Alzheimer Disease?Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- α-Methyl-α-phenylsuccinimide ameliorates neurodegeneration in a C. elegans model of TDP-43 proteinopathy.Neurobiology of disease · 2018Article
- Translational Geroscience: From invertebrate models to companion animal and human interventions.Translational medicine of aging · 2018Article
- Dianxianning improved amyloid β-induced pathological characteristics partially through DAF-2/DAF-16 insulin like pathway in transgenic C. elegans.Scientific reports · 2017Article
- Long-term Ameliorative Effects of the Antidepressant Fluoxetine Exposure on Cognitive Deficits in 3 × TgAD Mice.Molecular neurobiology · 2017Article
- The Atypical Antipsychotic Agent, Clozapine, Protects Against Corticosterone-Induced Death of PC12 Cells by Regulating the Akt/FoxO3a Signaling Pathway.Molecular neurobiology · 2017Article
- The stress response factor daf-16/FOXO is required for multiple compound families to prolong the function of neurons with Huntington's disease.Scientific reports · 2017Article
- Article
- Six psychotropics for pre-symptomatic & early Alzheimer's (MCI), Parkinson's, and Huntington's disease modification.Neural regeneration research · 2016Review
- An overview on therapeutics attenuating amyloid β level in Alzheimer's disease: targeting neurotransmission, inflammation, oxidative stress and enhanced cholesterol levels.American journal of translational research · 2016Review
- Using C. elegans to discover therapeutic compounds for ageing-associated neurodegenerative diseases.Chemistry Central journal · 2015Review
- Dopamine signaling in C. elegans is mediated in part by HLH-17-dependent regulation of extracellular dopamine levels.G3 (Bethesda, Md.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the most common form of dementia in elderly people. The accumulation of amyloid beta (Abeta) is one of the histopathological hallmarks of AD. Abeta is aggregated to form oligomers which are toxic to neurons and are critical to the onset and progression of AD. In a Caenorhabditis elegans (C. elegans) model of AD, human Abeta is expressed intracellularly in the body wall muscle. The expression and subsequent aggregation of Abeta in the muscle lead to progressive paralysis. Although the mechanism of action is unknown, antidepressants have been used with FDA approved drugs for dementia in AD and have been shown to enhance cognitive function in human and in animal models of AD. We found that the antidepressant fluoxetine, a selective serotonin reuptake inhibitor, significantly delayed Abeta-induced paralysis in the C. elegans model of Abeta toxicity by reducing Abeta oligomers. Our results showed that insulin signaling and DAF-16/FOXO transcription factors were required for fluoxetine-mediated delayed paralysis. We also found that fluoxetine increased thermal stress resistance and extended life span. These findings suggests that fluoxetine may have benefit for the treatment of AD by the reduction of proteotoxicity.
Indexed as
Identifiers
What OpenQuestion holds
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.