Evidence map›Paper›PMID 38356322›Full record

ArticleAnnals of neurology2024

Microglial Reactivity Correlates with Presynaptic Loss Independent of β-Amyloid and Tau.

Guoyu Lan, Xuhui Chen, Jie Yang, Pan Sun, Yue Cai, Anqi Li, Yalin Zhu, Zhen Liu, Shaohua Ma, Tengfei Guo and 1 more

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025
    Review
  8. Article
  9. Article
  10. Plasma N-terminal tau fragment is an amyloid-dependent biomarker in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  11. Mapping microglial mechanisms in Alzheimer's disease: a comprehensive analysis.Experimental biology and medicine (Maywood, N.J.) · 2025
    Article
  12. Review
  13. 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

11 authors at 3 institutions in 1 country.

Guoyu LanShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Xuhui ChenDepartment of Neurology, Peking University Shenzhen Hospital, Shenzhen, China.
Jie YangShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Pan SunShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Yue CaiShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Anqi LiShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Yalin ZhuShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Zhen LiuShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.
Shaohua MaTsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, China.
Tengfei GuoShenzhen Bay Laboratory, Institute of Biomedical Engineering, Shenzhen, China.ORCID 0000-0003-2982-0865
Alzheimer's Disease Neuroimaging Initiative
Shenzhen Bay Laboratory · CNPeking University Shenzhen Hospital · CNTsinghua–Berkeley Shenzhen Institute · CN

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI Duygu Tosun-Turgut · 2016 to 2026
$226.7M
Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
NIA NIH HHS U01 AG024904NIA NIH HHS U19 AG024904
6 · The paper itself

Abstract

objectiveTriggering receptor expressed on myeloid cells-2 (TREM2) and progranulin (PGRN) are critical regulators of microglia activation and can be detected in cerebrospinal fluid (CSF). However, whether microglial reactivity is detrimental or neuroprotective for Alzheimer disease (AD) is still debatable.

methodsWe identified 663 participants with baseline β-amyloid (Aβ) positron emission tomography (PET) and CSF biomarker data, including phosphorylated tau181 (p-Tau

resultsHigher baseline levels of CSF microglial biomarkers were related to faster rates of CSF sTREM2 increase and CSF PGRN decrease. Elevated CSF p-Tau

interpretationThese findings suggest that higher Aβ burden may attenuate the p-Tau-associated microglial responses, and TREM2-related microglial reactivity may independently correlate with GAP-43-related presynaptic loss. This study highlights the two-edged role of microglial reactivity in AD and other neurodegenerative diseases. ANN NEUROL 2024;95:917-928.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesMembrane GlycoproteinsMicrogliaPositron-Emission TomographyProgranulinsReceptors, Immunologictau ProteinsAgedAged, 80 and overBiomarkersCross-Sectional StudiesFemaleHumansLongitudinal StudiesMaleAmyloid beta-PeptidesBiomarkersGRN protein, humanMembrane GlycoproteinsProgranulinsReceptors, Immunologictau ProteinsTREM2 protein, human

Identifiers

PMID38356322
PMCPMC11060909
OpenAlexW4391841411

What OpenQuestion holds

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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.