Evidence map›Paper›PMID 38195627›Full record

ArticleNature communications2024

The aging mouse CNS is protected by an autophagy-dependent microglia population promoted by IL-34.

Rasmus Berglund, Yufei Cheng, Eliane Piket, Milena Z Adzemovic, Manuel Zeitelhofer, Tomas Olsson, Andre Ortlieb Guerreiro-Cacais, Maja Jagodic

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
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.

Rasmus BerglundDepartment of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden. rasmus.berglund@ki.se.ORCID 0000-0003-0252-7730
Yufei ChengDepartment of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.
Eliane PiketDepartment of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.
Milena Z AdzemovicDepartment of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.
Manuel ZeitelhoferDepartment of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institutet, 171 65, Solna, Sweden.ORCID 0000-0002-4324-2355
Tomas Olsson *Department of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.
Andre Ortlieb Guerreiro-Cacais *Department of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.ORCID 0000-0002-4561-2823
Maja Jagodic *Department of Clinical Neuroscience, Division of Neuro, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76, Stockholm, Sweden.ORCID 0000-0003-0756-889X
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) No 818170
6 · The paper itself

Abstract

Microglia harness an unutilized health-promoting potential in age-related neurodegenerative and neuroinflammatory diseases, conditions like progressive multiple sclerosis (MS). Our research unveils an microglia population emerging in the cortical brain regions of aging mice, marked by ERK1/2, Akt, and AMPK phosphorylation patterns and a transcriptome indicative of activated autophagy - a process critical for cellular adaptability. By deleting the core autophagy gene Ulk1 in microglia, we reduce this population in the central nervous system of aged mice. Notably, this population is found dependent on IL-34, rather than CSF1, although both are ligands for CSF1R. When aging mice are exposed to autoimmune neuroinflammation, the loss of autophagy-dependent microglia leads to neural and glial cell death and increased mortality. Conversely, microglial expansion mediated by IL-34 exhibits a protective effect. These findings shed light on an autophagy-dependent neuroprotective microglia population as a potential target for treating age-related neuroinflammatory conditions, including progressive MS.

Indexed as

Central Nervous SystemMicrogliaAnimalsAutophagyInterleukinsMiceNeurogliaInterleukins

Identifiers

PMID38195627
PMCPMC10776874
OpenAlexW4390793814

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.