Evidence map›Paper›PMID 38263055›Full record

ReviewMolecular brain2024

The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology.

Roberta Amoriello, Christian Memo, Laura Ballerini, Clara Ballerini

Open access · goldAbstract readReview
In one paragraph

Review in Molecular brain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Investigations of remibrutinib in models pertinent to multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Neuroprotective Pathway Modulation by a NovelInternational journal of molecular sciences · 2025
    Article
  11. Real-world effectiveness and safety of ofatumumab in relapsing-remitting multiple sclerosis: Insights from naïve and switch patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Article
  18. Review
  19. Review
  20. 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

4 authors at 2 institutions in 1 country.

Roberta AmorielloInternational School for Advanced Studies (SISSA/ISAS), 34136, Trieste, Italy. roberta.amoriello@unifi.it.ORCID 0000-0003-4356-3631
Christian MemoDipartimento di Medicina Sperimentale e Clinica, University of Florence, 50139, Florence, Italy.
Laura BalleriniDipartimento di Medicina Sperimentale e Clinica, University of Florence, 50139, Florence, Italy.
Clara BalleriniInternational School for Advanced Studies (SISSA/ISAS), 34136, Trieste, Italy. clara.ballerini@unifi.it.
Scuola Internazionale Superiore di Studi Avanzati · ITUniversity of Florence · IT

Funding

National Recovery and Resilience Plan (NRRP), project MNESYS PE0000006
6 · The paper itself

Abstract

The central nervous system (CNS) is finely protected by the blood-brain barrier (BBB). Immune soluble factors such as cytokines (CKs) are normally produced in the CNS, contributing to physiological immunosurveillance and homeostatic synaptic scaling. CKs are peptide, pleiotropic molecules involved in a broad range of cellular functions, with a pivotal role in resolving the inflammation and promoting tissue healing. However, pro-inflammatory CKs can exert a detrimental effect in pathological conditions, spreading the damage. In the inflamed CNS, CKs recruit immune cells, stimulate the local production of other inflammatory mediators, and promote synaptic dysfunction. Our understanding of neuroinflammation in humans owes much to the study of multiple sclerosis (MS), the most common autoimmune and demyelinating disease, in which autoreactive T cells migrate from the periphery to the CNS after the encounter with a still unknown antigen. CNS-infiltrating T cells produce pro-inflammatory CKs that aggravate local demyelination and neurodegeneration. This review aims to recapitulate the state of the art about CKs role in the healthy and inflamed CNS, with focus on recent advances bridging the study of adaptive immune system and neurophysiology.

Indexed as

Multiple SclerosisBrainCentral Nervous SystemCytokinesHumansNeuroinflammatory DiseasesCytokinesChemokinesCytokinesExperimental autoimmune encephalomyelitisMultiple SclerosisNeuroinflammationNeuromodulationSynaptopathy

Identifiers

PMID38263055
PMCPMC10807071
OpenAlexW4391132810

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.