Evidence map›Paper›PMID 38928248›Full record

SynthesisInternational journal of molecular sciences2024

Emerging Therapeutic Potential of Fluoxetine on Cognitive Decline in Alzheimer's Disease: Systematic Review.

Anastasia Bougea, Efthalia Angelopoulou, Efthimios Vasilopoulos, Philippos Gourzis, Sokratis Papageorgiou

Abstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Boosting Neurogenesis as a Strategy in Treating Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Anastasia Bougea1st Department of Neurology, "Aiginition" Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.ORCID 0000-0003-3006-8711
Efthalia Angelopoulou1st Department of Neurology, "Aiginition" Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.ORCID 0000-0002-1426-3384
Efthimios VasilopoulosFirst Department of Psychiatry, "Aiginition" Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.
Philippos GourzisFirst Department of Psychiatry, "Aiginition" Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.
Sokratis Papageorgiou1st Department of Neurology, "Aiginition" Hospital, School of Medicine, National and Kapodistrian University of Athens, 11528 Athens, Greece.ORCID 0000-0001-8863-3635

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fluoxetine, a commonly prescribed medication for depression, has been studied in Alzheimer's disease (AD) patients for its effectiveness on cognitive symptoms. The aim of this systematic review is to investigate the therapeutic potential of fluoxetine in cognitive decline in AD, focusing on its anti-degenerative mechanisms of action and clinical implications. According to PRISMA, we searched MEDLINE, up to 1 April 2024, for animal and human studies examining the efficacy of fluoxetine with regard to the recovery of cognitive function in AD. Methodological quality was evaluated using the ARRIVE tool for animal AD studies and the Cochrane tool for clinical trials. In total, 22 studies were analyzed (19 animal AD studies and 3 clinical studies). Fluoxetine promoted neurogenesis and enhanced synaptic plasticity in preclinical models of AD, through a decrease in Aβ pathology and increase in BDNF, by activating diverse pathways (such as the DAF-16-mediated, TGF-beta1, ILK-AKT-GSK3beta, and CREB/p-CREB/BDNF). In addition, fluoxetine has anti-inflammatory properties/antioxidant effects via targeting antioxidant Nrf2/HO-1 and hindering TLR4/NLRP3 inflammasome. Only three clinical studies showed that fluoxetine ameliorated the cognitive performance of people with AD; however, several methodological issues limited the generalizability of these results. Overall, the high-quality preclinical evidence suggests that fluoxetine may have neuroprotective, antioxidant, and anti-inflammatory effects in AD animal models. While more high-quality clinical research is needed to fully understand the mechanisms underlying these effects, fluoxetine is a promising potential treatment for AD patients. If future clinical trials confirm its anti-degenerative and neuroprotective effects, fluoxetine could offer a new therapeutic approach for slowing down the progression of AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionFluoxetineAnimalsDisease Models, AnimalHumansNeurogenesisNeuronal PlasticityFluoxetineAlzheimer’s diseaseBDNFcognitive declinefluoxetineneurogenesis

Identifiers

PMID38928248
PMCPMC11203451

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.