Evidence map›Paper›PMID 25472798›Full record

ArticleBrain : a journal of neurology2015

Neutralization of TNFSF10 ameliorates functional outcome in a murine model of Alzheimer's disease.

Giuseppina Cantarella, Giulia Di Benedetto, Daniela Puzzo, Lucia Privitera, Carla Loreto, Salvatore Saccone, Salvatore Giunta, Agostino Palmeri, Renato Bernardini

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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  11. 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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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Giuseppina Cantarella1 Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, University of Catania, 95125 Catania, Italy.
Giulia Di Benedetto1 Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, University of Catania, 95125 Catania, Italy 2 Li-Sa Laboratory, Department of Experimental Medicine, Section of Medical Physiopathology, Endocrinology and Nutrition, University of Roma 'La Sapienza', 00161 Rome, Italy.
Daniela Puzzo3 Department of Bio-Medical Sciences, Section of Physiology, University of Catania, 95125 Catania, Italy.
Lucia Privitera3 Department of Bio-Medical Sciences, Section of Physiology, University of Catania, 95125 Catania, Italy.
Carla Loreto4 Department of Bio-Medical Sciences, Section of Anatomy and Histology, University of Catania, 95125 Catania, Italy.
Salvatore Saccone5 Department of Biological, Geological and Environmental Sciences, Section of Animal Biology, University of Catania, 95125 Catania, Italy.
Salvatore Giunta4 Department of Bio-Medical Sciences, Section of Anatomy and Histology, University of Catania, 95125 Catania, Italy.
Agostino Palmeri3 Department of Bio-Medical Sciences, Section of Physiology, University of Catania, 95125 Catania, Italy.
Renato Bernardini1 Department of Clinical and Molecular Biomedicine, Section of Pharmacology and Biochemistry, University of Catania, 95125 Catania, Italy bernardi@unict.it.
University of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is one of the most common causes of death worldwide, with poor treatment options. A tissue landmark of Alzheimer's disease is accumulation of the anomalous protein amyloid-β in specific brain areas. Whether inflammation is an effect of amyloid-β on the Alzheimer's disease brain, or rather it represents a cause for formation of amyloid plaques and intracellular tangles remains a subject of debate. TNFSF10, a proapoptotic cytokine of the TNF superfamily, is a mediator of amyloid-β neurotoxicity. Here, we demonstrate that blocking TNFSF10 by administration of a neutralizing monoclonal antibody could attenuate the amyloid-β-induced neurotoxicity in a triple transgenic mouse model of Alzheimer's disease (3xTg-AD). The effects of TNFSF10 neutralization on either cognitive parameters, as well as on the expression of TNFSF10, amyloid-β, inflammatory mediators and GFAP were studied in the hippocampus of 3xTg-AD mice. Treatment with the TNFSF10 neutralizing antibody resulted in dramatic improvement of cognitive parameters, as assessed by the Morris water maze test and the novel object recognition test. These results were correlated with decreased protein expression of TNFSF10, amyloid-β, inflammatory mediators and GFAP in the hippocampus. Finally, neutralization of TNFSF10 results in functional improvement and restrained immune/inflammatory response in the brain of 3xTg-AD mice in vivo. Thus, it is plausible to regard the TNFSF10 system as a potential target for efficacious treatment of amyloid-related disorders.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAntibodies, MonoclonalCognition DisordersDisease Models, AnimalGene Expression RegulationGliosisHippocampusHumansMaleMaze LearningMemoryMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAntibodies, MonoclonalPresenilin-1PSEN1 protein, humantau ProteinsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanamyloid-βhippocampusinflammationneurodegenerationTNFSF10

Identifiers

PMID25472798
PMCPMC4441080
OpenAlexW2139663796

What OpenQuestion holds

Textmetadata
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.