Evidence map›Paper›PMID 33050925›Full record

ReviewJournal of neuroinflammation2020

The immune system on the TRAIL of Alzheimer's disease.

Chiara Burgaletto, Antonio Munafò, Giulia Di Benedetto, Cettina De Francisci, Filippo Caraci, Rosaria Di Mauro, Claudio Bucolo, Renato Bernardini, Giuseppina Cantarella

Open access · goldAbstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.5field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  7. Review
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  13. Rebalancing Immune Interactions within the Brain-Spleen Axis Mitigates Neuroinflammation in an Aging Mouse Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

9 authors at 2 institutions in 1 country.

Chiara BurgalettoDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Antonio MunafòDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Giulia Di BenedettoDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Cettina De FrancisciDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Filippo CaraciDepartment of Drug Sciences, University of Catania, Catania, Italy.
Rosaria Di MauroDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Claudio BucoloDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
Renato BernardiniDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy. bernardi@unict.it.
Giuseppina CantarellaDepartment of Biomedical and Biotechnological Sciences (BIOMETEC), Section of Pharmacology, University of Catania, Via Santa Sofia 97, Catania, Italy.
University of Catania · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

PRIN grant from the Italian Ministry of Research 2017YH3SXK
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive degeneration and loss of neurons in specific regions of the central nervous system. Chronic activation of the immune cells resident in the brain, peripheral immune cell trafficking across the blood-brain barrier, and release of inflammatory and neurotoxic factors, appear critical contributors of the neuroinflammatory response that drives the progression of neurodegenerative processes in AD. As the neuro-immune network is impaired in course of AD, this review is aimed to point out the essential supportive role of innate and adaptive immune response either in normal brain as well as in brain recovery from injury. Since a fine-tuning of the immune response appears crucial to ensure proper nervous system functioning, we focused on the role of the TNF superfamily member, TNF-related apoptosis-inducing ligand (TRAIL), which modulates both the innate and adaptive immune response in the pathogenesis of several immunological disorders and, in particular, in AD-related neuroinflammation. We here summarized mounting evidence of potential involvement of TRAIL signaling in AD pathogenesis, with the aim to provide clearer insights about potential novel therapeutic approaches in AD.

Indexed as

Alzheimer DiseaseAnimalsBrainHumansImmunity, CellularTNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanImmune responseNeuroinflammationProinflammatory cytokinesRegulatory T cells

Identifiers

PMID33050925
PMCPMC7556967
OpenAlexW3092017418

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.