Evidence map›Paper›PMID 36661537›Full record

ArticleCurrent issues in molecular biology2023

1,2-

Ginevra Giacomello, Carolin Otto, Josef Priller, Klemens Ruprecht, Chotima Böttcher, Maria Kristina Parr

Open access · goldAbstract read
In one paragraph

Article in Current issues in molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Glycolytic metabolism: Food for immune cells, fuel for depression?Brain, behavior, & immunity - health · 2024
    Article
  5. Review
  6. 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

6 authors at 4 institutions in 2 countries.

Ginevra GiacomelloInstitute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2 + 4, 14195 Berlin, Germany.ORCID 0000-0002-0914-4241
Carolin OttoDepartment of Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Josef PrillerDepartment of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Klemens RuprechtDepartment of Neurology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Chotima BöttcherDepartment of Neuropsychiatry and Laboratory of Molecular Psychiatry, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Maria Kristina ParrInstitute of Pharmacy, Freie Universität Berlin, Königin-Luise-Str. 2 + 4, 14195 Berlin, Germany.ORCID 0000-0001-7407-8300
Freie Universität Berlin · DEHumboldt-Universität zu Berlin · DEGerman Center for Neurodegenerative Diseases · DEMax Delbrück Center · DE

Funding

Deutsche Forschungsgemeinschaft 259373024 - CRC/TRR 167 (B05).European Union 821283-2Freie Universität Berlin The publication of this article was funded by Freie Universität BerliState of Berlin, Germany, Elsa-Neumann Ph.D. scholarship 069032
6 · The paper itself

Abstract

Neuroinflammation is one of the common features in most neurological diseases including multiple sclerosis (MScl) and neurodegenerative diseases such as Alzheimer's disease (AD). It is associated with local brain inflammation, microglial activation, and infiltration of peripheral immune cells into cerebrospinal fluid (CSF) and the central nervous system (CNS). It has been shown that the diversity of phenotypic changes in monocytes in CSF relates to neuroinflammation. It remains to be investigated whether these phenotypic changes are associated with functional or metabolic alteration, which may give a hint to their function or changes in cell states, e.g., cell activation. In this article, we investigate whether major metabolic pathways of blood monocytes alter after exposure to CSF of healthy individuals or patients with AD or MScl. Our findings show a significant alteration of the metabolism of monocytes treated with CSF from patients and healthy donors, including higher production of citric acid and glutamine, suggesting a more active glycolysis and tricarboxylic acid (TCA) cycle and reduced production of glycine and serine. These alterations suggest metabolic reprogramming of monocytes, possibly related to the change of compartment (from blood to CSF) and/or disease-related. Moreover, the levels of serine differ between AD and MScl, suggesting different phenotypic alterations between diseases.

Indexed as

Alzheimercerebrospinal fluidglycolysismetabolismmetabolitesmonocytesmultiple sclerosisneuroinflammationtricarboxylic acid cycle

Identifiers

PMID36661537
PMCPMC9857935
OpenAlexW4316469473

What Socratic 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 Socratic graph.