Evidence map›Paper›PMID 36928859›Full record

ArticleAdvances in neurobiology2023

Increased Inflammation and Treatment of Depression: From Resistance to Reuse, Repurposing, and Redesign.

Jennifer C Felger

Abstract read
PubMed Publisher
In one paragraph

Article in Advances in neurobiology, 2023. 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
1.9field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

1 author at 1 institution in 1 country.

Jennifer C FelgerEmory University School of Medicine, Atlanta, GA, USA. jfelger@emory.edu.
Emory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Based on mounting clinical and translational evidence demonstrating the impact of exogenously administered inflammatory stimuli on the brain and behavior, increased endogenous inflammation has received attention as one pathophysiologic process contributing to psychiatric illnesses and particularly depression. Increased endogenous inflammation is observed in a significant proportion of depressed patients and has been associated with reduced responsiveness to standard antidepressant therapies. This chapter presents recent evidence that inflammation affects neurotransmitters and neurocircuits to contribute to specific depressive symptoms including anhedonia, motor slowing, and anxiety, which may preferentially improve after anti-cytokine therapies in patients with evidence of increased inflammation. Existing and novel pharmacological strategies that target inflammation or its downstream effects on the brain and behavior will be discussed in the context of a need for intelligent trial design in order to meaningfully translate these concepts and develop more precise therapies for depressed patients with increased inflammation.

Indexed as

BrainDepressionAntidepressive AgentsAnxiety DisordersHumansInflammationAntidepressive AgentsAnhedoniaAntidepressantsCytokinesDepressionDopamineGlutamateInflammation

Identifiers

PMID36928859
OpenAlexW4327654355

What OpenQuestion holds

Textmetadata
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.