Evidence map›Paper›PMID 26255886›Full record

ArticleAging cell2015

Atypical antidepressants extend lifespan of Caenorhabditis elegans by activation of a non-cell-autonomous stress response.

Sunitha Rangaraju, Gregory M Solis, Sofia I Andersson, Rafael L Gomez-Amaro, Rozina Kardakaris, Caroline D Broaddus, Alexander B Niculescu, Michael Petrascheck

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 32% of its field
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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Premature aging in serious mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

8 authors at 2 institutions in 1 country.

Sunitha RangarajuDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Gregory M SolisDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Sofia I AnderssonDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Rafael L Gomez-AmaroDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Rozina KardakarisDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Caroline D BroaddusDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Alexander B NiculescuDepartment of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, USA.
Michael PetrascheckDepartment of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA.
Scripps Research Institute · USIndiana University School of Medicine

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Modulation of Sensory Perception to Treat Age Related DiseaseDP2OD008398 · OD · SCRIPPS RESEARCH INSTITUTE, THE · PI PETRASCHECK, MICHAEL · 2011 to 2011
$2.8M
NIH HHS DP2 OD008398NIH HHS P40 OD010440
6 · The paper itself

Abstract

Oxidative stress has long been associated with aging and has recently been linked to psychiatric disorders, including psychosis and depression. We identified multiple antipsychotics and antidepressants that extend Caenorhabditis elegans lifespan and protect the animal from oxidative stress. Here, we report that atypical antidepressants activate a neuronal mechanism that regulates the response to oxidative stress throughout the animal. While the activation of the oxidative stress response by atypical antidepressants depends on synaptic transmission, the activation by reactive oxygen species does not. Lifespan extension by atypical antidepressants depends on the neuronal oxidative stress response activation mechanism. Neuronal regulation of the oxidative stress response is likely to have evolved as a survival mechanism to protect the organism from oxidative stress, upon detection of adverse or dangerous conditions by the nervous system.

Indexed as

Life ExpectancyAgingAnimalsAntidepressive Agents, Second-GenerationCaenorhabditis elegansCaenorhabditis elegans ProteinsCatalaseFluoxetineHistamine H1 AntagonistsLongevityMianserinMirtazapineOxidative StressPeroxiredoxinsReactive Oxygen SpeciesSelective Serotonin Reuptake InhibitorsAntidepressive Agents, Second-GenerationCaenorhabditis elegans ProteinsCatalaseFluoxetineHistamine H1 AntagonistsMianserinMirtazapinePeroxiredoxinsPRDX-2 protein, C elegansReactive Oxygen SpeciesSelective Serotonin Reuptake InhibitorsSerotonin AntagonistsSod-1 protein, C elegansSuperoxide Dismutaseanti-agingantidepressantCaenorhabditis elegansnon-cell-autonomouspsychiatric diseasesignal transductionstresssynaptic transmission

Identifiers

PMID26255886
PMCPMC4693466
OpenAlexW2129182381

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.