Evidence map›Paper›PMID 33803478›Full record

ArticleInternational journal of molecular sciences2021

Microglial Heterogeneity and Its Potential Role in Driving Phenotypic Diversity of Alzheimer's Disease.

Stefano Sorrentino, Roberto Ascari, Emanuela Maderna, Marcella Catania, Bernardino Ghetti, Fabrizio Tagliavini, Giorgio Giaccone, Giuseppe Di Fede

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  6. Chronic palmitoylethanolamide administrationFrontiers in cellular neuroscience · 2025
    Article
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  8. Article
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  12. Recent update on the heterogeneity of the Alzheimer's disease spectrum.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
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  15. Article
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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 2 countries.

Stefano SorrentinoCNR NANOTEC-Institute of Nanotechnology, 73100 Lecce, Italy.ORCID 0000-0002-5833-5183
Roberto AscariDepartment of Economics, Management, and Statistics (DEMS)-University of Milano-Bicocca, 20126 Milan, Italy.ORCID 0000-0003-0146-976X
Emanuela MadernaNeurology 5 and Neuropathology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy.ORCID 0000-0002-5736-3166
Marcella CataniaNeurology 5 and Neuropathology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy.ORCID 0000-0003-0370-1905
Bernardino GhettiDepartment of Pathology and Laboratory Medicine, Indiana University, Indianapolis, IN 46202, USA.
Fabrizio TagliaviniScientific Directorate, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy.
Giorgio GiacconeNeurology 5 and Neuropathology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy.
Giuseppe Di FedeNeurology 5 and Neuropathology Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, 20133 Milan, Italy.ORCID 0000-0003-3537-6713
Fondazione IRCCS Istituto Neurologico Carlo Besta · ITIndiana University – Purdue University Indianapolis · USIstituto di Nanotecnologia · ITUniversity of Milano-Bicocca · IT

Funding

EU Joint Programme - Neurodegenerative Disease Research REfrAMEMinistero della Salute RC 2018-20
6 · The paper itself

Abstract

Alzheimer's disease (AD) is increasingly recognized as a highly heterogeneous disorder occurring under distinct clinical and neuropathological phenotypes. Despite the molecular determinants of such variability not being well defined yet, microglial cells may play a key role in this process by releasing distinct pro- and/or anti-inflammatory cytokines, potentially affecting the expression of the disease. We carried out a neuropathological and biochemical analysis on a series of AD brain samples, gathering evidence about the heterogeneous involvement of microglia in AD. The neuropathological studies showed differences concerning morphology, density and distribution of microglial cells among AD brains. Biochemical investigations showed increased brain levels of IL-4, IL-6, IL-13, CCL17, MMP-7 and CXCL13 in AD in comparison with control subjects. The molecular profiling achieved by measuring the brain levels of 25 inflammatory factors known to be involved in neuroinflammation allowed a stratification of the AD patients in three distinct "neuroinflammatory clusters". These findings strengthen the relevance of neuroinflammation in AD pathogenesis suggesting, in particular, that the differential involvement of neuroinflammatory molecules released by microglial cells during the development of the disease may contribute to modulate the characteristics and the severity of the neuropathological changes, driving-at least in part-the AD phenotypic diversity.

Indexed as

Alzheimer DiseaseBrainCytokinesHumansInflammationMicrogliaCytokinesAlzheimer’s diseaseAβchemokinescytokinesdementiaheterogeneityinnate immunity factorsmicrogliaMMPsneuroinflammation

Identifiers

PMID33803478
PMCPMC7967159
OpenAlexW3134463211

What OpenQuestion holds

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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.