Evidence map›Paper›PMID 11927634›Full record

ArticleThe Journal of experimental medicine2002

Role of p75 neurotrophin receptor in the neurotoxicity by beta-amyloid peptides and synergistic effect of inflammatory cytokines.

Giovanni Perini, Vittorina Della-Bianca, Valeria Politi, Giuliano Della Valle, Ilaria Dal-Pra, Filippo Rossi, Ubaldo Armato

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 150 citations in OpenAlex.

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  16. Cellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer's Disease.International journal of molecular sciences · 2018
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Giovanni PeriniDepartment of Biology, University of Bologna, Via Selmi 3, 40126 Bologna, Italy.
Vittorina Della-Bianca
Valeria Politi
Giuliano Della Valle
Ilaria Dal-Pra
Filippo Rossi
Ubaldo Armato
University of Bologna · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neurodegenerative changes in Alzheimer's disease (AD) are elicited by the accumulation of beta-amyloid peptides (Abeta), which damage neurons either directly by interacting with components of the cell surface to trigger cell death signaling or indirectly by activating astrocytes and microglia to produce inflammatory mediators. It has been recently proposed that the p75 neurotrophin receptor (p75(NTR)) is responsible for neuronal damage by interacting with Abeta. By using neuroblastoma cell clones lacking the expression of all neurotrophin receptors or engineered to express full-length or various truncated forms of p75(NTR), we could show that p75(NTR) is involved in the direct signaling of cell death by Abeta via the function of its death domain. This signaling leads to the activation of caspases-8 and -3, the production of reactive oxygen intermediates and the induction of an oxidative stress. We also found that the direct and indirect (inflammatory) mechanisms of neuronal damage by Abeta could act synergistically. In fact, TNF-alpha and IL-1beta, cytokines produced by Abeta-activated microglia, could potentiate the neurotoxic action of Abeta mediated by p75(NTR) signaling. Together, our results indicate that neurons expressing p75(NTR), mostly if expressing also proinflammatory cytokine receptors, might be preferential targets of the cytotoxic action of Abeta in AD.

Indexed as

Amyloid beta-PeptidesCell SurvivalClone CellsCytokinesDrug SynergismGene Expression RegulationHumansKineticsNeuroblastomaNeuronsNeurotoxinsPeptide FragmentsReceptor, Nerve Growth FactorReceptors, Nerve Growth FactorReceptor, trkARecombinant ProteinsAmyloid beta-PeptidesCytokinesNeurotoxinsPeptide FragmentsReceptor, Nerve Growth FactorReceptors, Nerve Growth FactorReceptor, trkARecombinant Proteins

Identifiers

PMID11927634
PMCPMC2193732
OpenAlexW2142819123

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.