Evidence map›Paper›PMID 34751640›Full record

ReviewPrion2021

The role of microglia in prion diseases and possible therapeutic targets: a literature review.

Ananda Sampaio Lamenha Falcão de Melo, Juliana Louise Dias Lima, Maria Carolina Silva Malta, Natália França Marroquim, Álvaro Rivelli Moreira, Isabelle de Almeida Ladeia, Fabrizio Dos Santos Cardoso, Daniel Buzaglo Gonçalves, Bruna Guimarães Dutra, Júlio César Claudino Dos Santos

Open access · goldAbstract readReview
In one paragraph

Review in Prion, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Neuroglial P2YJournal of neuroinflammation · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Prion diseases: Lessons from historical outbreaks and potential emerging ones.Protein science : a publication of the Protein Society · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. 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

10 authors at 4 institutions in 2 countries.

Ananda Sampaio Lamenha Falcão de MeloFaculdade de Medicina, Universidade Federal de Alagoas, Alagoas, AL, Brazil.
Juliana Louise Dias LimaFaculdade de Medicina, Universidade Federal de Alagoas, Alagoas, AL, Brazil.
Maria Carolina Silva MaltaFaculdade de Medicina, Universidade Federal de Alagoas, Alagoas, AL, Brazil.
Natália França MarroquimFaculdade de Medicina, Universidade Federal de Alagoas, Alagoas, AL, Brazil.
Álvaro Rivelli MoreiraDepartment of Neurology, Centro Universitário Governador Ozanam Coelho, UniFacog, Ubá, MG, Brazil.
Isabelle de Almeida LadeiaDepartment of Neurology, Centro Universitário Governador Ozanam Coelho, UniFacog, Ubá, MG, Brazil.
Fabrizio Dos Santos CardosoNúcleo de Pesquisas Tecnológicas, Universidade De Mogi Das Cruzes, Mogi das Cruzes, SP, Brazil.
Daniel Buzaglo GonçalvesUniversidade Federal do Amazonas, Ubá, AM, Brazil.ORCID 0000-0002-3243-970X
Bruna Guimarães DutraUniversidade Federal do Amazonas, Ubá, AM, Brazil.
Júlio César Claudino Dos SantosLaboratório de Neurociências, Departamento De Neurologia E Neurocirurgia, Universidade Federal de São Paulo, São Paulo, Sp, Brazil.
Universidade Federal de Alagoas · BRUniversidade Federal do Amazonas · BRSociedade Brasileira de Neurociências e Comportamento · BRThe University of Texas at Austin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Creutzfeldt-Jakob disease (CJD) is a rare and fatal condition that leads to progressive neurodegeneration due to gliosis, vacuolation of central nervous system tissue, and loss of neurons. Microglia play a crucial role in maintaining Central Nervous System (CNS) homoeostasis, both in health and disease, through phagocytosis and cytokine production. In the context of CJD, the immunomodulatory function of microglia turns it into a cell of particular interest. Microglia would be activated by infectious prion proteins, initially acquiring a phagocytic and anti-inflammatory profile (M2), and producing cytokines such as IL-4, IL-10, and TGF-β. Therefore, microglia are seen as a key target for the development of new treatment approaches, with many emerging strategies to guide it towards a beneficial role upon neuroinflammation, by manipulating its metabolic pathways. In such a setting, many cellular targets in microglia that can be involved in phenotype modulation, such as membrane receptors, have been identified and pointed out as possible targets for further experiments and therapeutic approaches. In this article, we review the major findings about the role of microglia in CJD, including its relationship to some risk factors associated with the development of the disease. Furthermore, considering its central role in neural immunity, we explore microglial connection with other elements of the immune system and cell signalling, such as inflammasomes, the complement and purinergic systems, and the latest finding strategies to guide these cells from harmful to beneficial roles.

Indexed as

Creutzfeldt-Jakob SyndromePrion DiseasesPrionsCytokinesHumansMicrogliaCytokinesPrionsCreutzfeldt-Jakob diseasemicroglianeuroinflammation pathways

Identifiers

PMID34751640
PMCPMC8583147
OpenAlexW3214271799

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.