Evidence map›Paper›PMID 38927365›Full record

ArticleBiomedicines2024

Comparison of Protective Effects of Antidepressants Mediated by Serotonin Receptor in Aβ-Oligomer-Induced Neurotoxicity.

Ken Yamamoto, Mayumi Tsuji, Tatsunori Oguchi, Yutaro Momma, Hideaki Ohashi, Naohito Ito, Tetsuhito Nohara, Tatsuya Nakanishi, Atsushi Ishida, Masahiro Hosonuma and 3 more

Abstract read
In one paragraph

Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.International journal of physiology, pathophysiology and pharmacology · 2024
    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

13 authors.

Ken YamamotoDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Mayumi TsujiPharmacological Research Center, Showa University, Tokyo 142-8555, Japan.ORCID 0000-0001-8005-9069
Tatsunori OguchiDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Yutaro MommaDepartment of Neurology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Hideaki OhashiDepartment of Neurology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Naohito ItoDepartment of Neurology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Tetsuhito NoharaDepartment of Neurology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Tatsuya NakanishiDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Atsushi IshidaDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Masahiro HosonumaDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Toru NishikawaDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.
Hidetomo MurakamiDepartment of Neurology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Yuji KiuchiDepartment of Pharmacology, Showa University Graduate School of Medicine, Tokyo 142-8555, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloid β-peptide (Aβ) synthesis and deposition are the primary factors underlying the pathophysiology of Alzheimer's disease (AD). Aβ oligomer (Aβo) exerts its neurotoxic effects by inducing oxidative stress and lesions by adhering to cellular membranes. Though several antidepressants have been investigated as neuroprotective agents in AD, a detailed comparison of their neuroprotection against Aβo-induced neurotoxicity is lacking. Here, we aimed to elucidate the neuroprotective effects of clinically prescribed selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and noradrenergic and specific serotonergic antidepressants at the cellular level and establish the underlying mechanisms for their potential clinical applications. Therefore, we compared the neuroprotective effects of three antidepressants, fluoxetine (Flx), duloxetine (Dlx), and mirtazapine (Mir), by their ability to prevent oxidative stress-induced cell damage, using SH-SY5Y cells, by evaluating cell viability, generation of reactive oxygen species (ROS) and mitochondrial ROS, and peroxidation of cell membrane phospholipids. These antidepressants exhibited potent antioxidant activity (Dlx > Mir > Flx) and improved cell viability. Furthermore, pretreatment with a 5-hydroxytryptamine 1A (5-HT

Indexed as

5-HT1A receptorAlzheimer’s diseaseamyloid β oligomerantidepressantsantioxidant

Identifiers

PMID38927365
PMCPMC11200737

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Registered trials

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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.