Evidence map›Paper›PMID 38575806›Full record

ReviewMolecular psychiatry2024

Ketamine's mechanism of action with an emphasis on neuroimmune regulation: can the complement system complement ketamine's antidepressant effects?

Brandi Quintanilla, Carlos A Zarate, Anilkumar Pillai

Open access · greenAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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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

3 authors at 3 institutions in 1 country.

Brandi QuintanillaPathophysiology of Neuropsychiatric Disorders Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA.
Carlos A ZarateExperimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA.
Anilkumar PillaiPathophysiology of Neuropsychiatric Disorders Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA. anilkumar.r.pillai@uth.tmc.edu.ORCID 0000-0002-1952-8556
Charlie Norwood VA Medical Center · USNational Institutes of Health · USThe University of Texas Health Science Center at Houston · US

Funding

Glutamatergic Modulators for Rapid & Sustained Antidepressant EffectZIAMH002857 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI ZARATE, CARLOS · 2009 to 2025
$55.0M
Complement Component, Neuroinflammation and DepressionR01MH120876 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI PILLAI, ANILKUMAR · 2019 to 2023
$1.9M
Mitochondrial DNA, chronic stress, and inflammationR56MH128771 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI PILLAI, ANILKUMAR · 2022 to 2023
$891k
Chronic stress, complement immune system and behaviorR21MH121959 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI PILLAI, ANILKUMAR · 2019 to 2020
$424k
BLRD VA I01 BX004758Intramural NIH HHS ZIA MH002857NIMH NIH HHS R01 MH120876NIMH NIH HHS R21 MH121959NIMH NIH HHS R56 MH128771U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) MH120876U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) MH121959U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (NIMH) MH128771U.S. Department of Veterans Affairs (Department of Veterans Affairs) BX004758
6 · The paper itself

Abstract

Over 300 million people worldwide suffer from major depressive disorder (MDD). Unfortunately, only 30-40% of patients with MDD achieve complete remission after conventional monoamine antidepressant therapy. In recent years, ketamine has revolutionized the treatment of MDD, with its rapid antidepressant effects manifesting within a few hours as opposed to weeks with conventional antidepressants. Many research endeavors have sought to identify ketamine's mechanism of action in mood disorders; while many studies have focused on ketamine's role in glutamatergic modulation, several studies have implicated its role in regulating neuroinflammation. The complement system is an important component of the innate immune response vital for synaptic plasticity. The complement system has been implicated in the pathophysiology of depression, and studies have shown increases in complement component 3 (C3) expression in the prefrontal cortex of suicidal individuals with depression. Given the role of the complement system in depression, ketamine and the complement system's abilities to modulate glutamatergic transmission, and our current understanding of ketamine's anti-inflammatory properties, there is reason to suspect a common link between the complement system and ketamine's mechanism of action. This review will summarize ketamine's anti- inflammatory roles in the periphery and central nervous system, with an emphasis on complement system regulation.

Indexed as

Antidepressive AgentsComplement System ProteinsKetamineMajor Depressive DisorderAnimalsHumansNeuroimmunomodulationPrefrontal CortexAntidepressive AgentsComplement System ProteinsKetamine

Identifiers

PMID38575806
PMCPMC11804209
OpenAlexW4393927030

What OpenQuestion holds

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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.