Evidence map›Paper›PMID 37543564›Full record

ReviewJournal of neuroinflammation2023

Lysosomal acidification dysfunction in microglia: an emerging pathogenic mechanism of neuroinflammation and neurodegeneration.

Joseph D Quick, Cristian Silva, Jia Hui Wong, Kah Leong Lim, Richard Reynolds, Anna M Barron, Jialiu Zeng, Chih Hung Lo

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
16.2field-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

116 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

56 more citing papers are in PubMed but not listed here.

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 4 institutions in 4 countries.

Joseph D QuickDepartment of Integrative Biology and Physiology, Medical School, University of Minnesota, Minneapolis, MN, USA.
Cristian SilvaFaculty of Graduate Studies, University of Kelaniya, Kelaniya, Sri Lanka.
Jia Hui WongLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
Kah Leong LimLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
Richard ReynoldsLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
Anna M BarronLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.
Jialiu ZengLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore. jialiu.zeng@ntu.edu.sg.
Chih Hung LoLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore. chihhung.lo@ntu.edu.sg.
Nanyang Technological University · SGImperial College London · GBUniversity of Kelaniya · LKUniversity of Minnesota Medical Center · US

Funding

Lee Kong Chian School of Medicine, Nanyang Technological University Dean's Postdoctoral Fellowship (Award Number: 021207-00001)Momental Foundation Mistletoe Research Fellowship (Award Number: 022522-00001)Nanyang Technological University Presidential Postdoctoral Fellowship (Award Number: 021229-00001)National Medical Research Council Open Fund Young Investigator Research Grant (OF-YIRG) (Award Number: MOH-001147)
6 · The paper itself

Abstract

Microglia are the resident innate immune cells in the brain with a major role in orchestrating immune responses. They also provide a frontline of host defense in the central nervous system (CNS) through their active phagocytic capability. Being a professional phagocyte, microglia participate in phagocytic and autophagic clearance of cellular waste and debris as well as toxic protein aggregates, which relies on optimal lysosomal acidification and function. Defective microglial lysosomal acidification leads to impaired phagocytic and autophagic functions which result in the perpetuation of neuroinflammation and progression of neurodegeneration. Reacidification of impaired lysosomes in microglia has been shown to reverse neurodegenerative pathology in Alzheimer's disease. In this review, we summarize key factors and mechanisms contributing to lysosomal acidification impairment and the associated phagocytic and autophagic dysfunction in microglia, and how these defects contribute to neuroinflammation and neurodegeneration. We further discuss techniques to monitor lysosomal pH and therapeutic agents that can reacidify impaired lysosomes in microglia under disease conditions. Finally, we propose future directions to investigate the role of microglial lysosomal acidification in lysosome-mitochondria crosstalk and in neuron-glia interaction for more comprehensive understanding of its broader CNS physiological and pathological implications.

Indexed as

Alzheimer DiseaseMicrogliaHumansHydrogen-Ion ConcentrationLysosomesNeuroinflammatory DiseasesAcidic nanoparticlesAutophagyCytokinesLysosomal acidificationNeurodegenerative diseasesNeuroinflammationPhagocytosisToxic protein aggregates

Identifiers

PMID37543564
PMCPMC10403868
OpenAlexW4385607049

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.