Evidence map›Paper›PMID 36058959›Full record

ReviewJournal of neuroinflammation2022

Pathogenesis, therapeutic strategies and biomarker development based on "omics" analysis related to microglia in Alzheimer's disease.

Chao Gao, Xin Shen, Yuyan Tan, Shengdi Chen

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
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  7. Article
  8. Review
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  12. Article
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  15. Article
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  17. Multiomics of Aging and Aging-Related Diseases.International journal of molecular sciences · 2024
    Review
  18. Review
  19. Review
  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

4 authors at 3 institutions in 1 country.

Chao Gao *Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Xin Shen *Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Yuyan TanDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. yuyantan00@126.com.
Shengdi ChenDepartment of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. chensd@rjh.com.cn.
Ruijin Hospital · CNShanghai Jiao Tong University · CNShanghaiTech University · CN

Funding

Innovation Program of Shanghai Municipal Education Commission 2017-01-07-00-01-E00046National Natural Science Foundation of China 82101477National Natural Science Foundation of China 82171401Shanghai Municipal Science and Technology Major Project Grant 2018SHZDZX05
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease and the most common cause of dementia. Among various pathophysiological aspects, microglia are considered to play important roles in the pathogenesis of AD. Genome wide association studies (GWAS) showed that the majority of AD risk genes are highly or exclusively expressed in microglia, underscoring the critical roles of microglia in AD pathogenesis. Recently, omics technologies have greatly advanced our knowledge of microglia biology in AD. Omics approaches, including genomics, epigenomics, transcriptomics, proteomics, and metabolomics/lipidomics, present remarkable opportunities to delineate the underlying mechanisms, discover novel diagnostic biomarkers, monitor disease progression, and shape therapeutic strategies for diseases. In this review, we summarized research based on microglial "omics" analysis in AD, especially the recent research advances in the identification of AD-associated microglial subsets. This review reinforces the important role of microglia in AD and advances our understanding of the mechanism of microglia in AD pathogenesis. Moreover, we proposed the value of microglia-based omics in the development of therapeutic strategies and biomarkers for AD.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesBiomarkersGenome-Wide Association StudyHumansMicrogliaBiomarkersAlzheimer’s diseaseBiomarkerMicrogliaOmicsPathogenesisTherapeutic strategy

Identifiers

PMID36058959
PMCPMC9441025
OpenAlexW4294555566

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.