Evidence map›Paper›PMID 33847763›Full record

ReviewCellular and molecular life sciences : CMLS2021

Cytokine signaling convergence regulates the microglial state transition in Alzheimer's disease.

Shun-Fat Lau, Amy K Y Fu, Nancy Y Ip

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Ferroptosis in depression: mechanisms, association, and therapeutic strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

3 authors at 1 institution in 3 countries.

Shun-Fat LauDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Amy K Y FuDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Nancy Y IpDivision of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China. boip@ust.hk.ORCID http://orcid.org/0000-0002-2763-8907
Hong Kong University of Science and Technology · HK

Funding

Innovation and Technology Commission - Hong Kong ITCPD/17-9Research Grants Council of Hong Kong C6027-19GFResearch Grants Council of Hong Kong HKUST16100418Research Grants Council of Hong Kong HKUST16102019Research Grants Council of Hong Kong HKUST16103017Research Grants Council of Hong Kong HKUST16149616Research Grants Council of Hong Kong T13-607/12RResearch Grants Council, University Grants Committee Hong Kong PhD Fellowship AwardShenzhen Knowledge Innovation Program Grants JCYJ20170413173717055Shenzhen Knowledge Innovation Program Grants JCYJ20180507183642005the Guangdong Provincial Key S&T Program Grant 2018B030336001the National Key R&D Program of China Grants 2017YFE0190000the National Key R&D Program of China Grants 2018YFE0203600University Grants Committee AoE/M-604/16
6 · The paper itself

Abstract

Genetic analyses have revealed the pivotal contribution of microglial dysfunctions to the pathogenesis of Alzheimer's disease (AD). Along AD progression, the accumulation of danger-associated molecular patterns (DAMPs) including beta-amyloid and hyperphosphorylated tau continuously stimulates microglia, which results in their chronic activation. Chronically activated microglia secrete excessive pro-inflammatory cytokines, which further regulate microglial responses towards DAMPs. This has spurred longstanding interest in targeting cytokine-induced microglial responses for AD therapeutic development. However, the cytokine-induced microglial state transition is not comprehensively understood. Cytokines are assumed to induce microglial state transition from a resting state to an activated state. However, recent evidence indicate that this microglial state transition involves multiple sequential functional states. Moreover, the mechanisms by which different functional states within the cytokine-induced microglial state transition regulate AD pathology remain unclear. In this review, we summarize how different cytokine signaling pathways, including those of IL-33 (interleukin-33), NLRP3 inflammasome-IL-1β, IL-10, and IL-12/IL-23, regulate microglial functions in AD. Furthermore, we discuss how the modulation of these cytokine signaling pathways can result in beneficial outcomes in AD. Finally, we describe a stepwise functional state transition of microglia induced by cytokine signaling that can provide insights into the molecular basis of the beneficial effects of cytokine modulation in AD and potentially aid therapeutic development.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCytokinesHumansInflammasomesMicrogliaSignal TransductionAmyloid beta-PeptidesCytokinesInflammasomesAmyloidChemotaxisInterleukinPhagocytosisTau

Identifiers

PMID33847763
PMCPMC8195901
OpenAlexW3155464689

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.