Evidence map›Paper›PMID 26042083›Full record

ReviewFrontiers in neurology2015

NF-κB in Innate Neuroprotection and Age-Related Neurodegenerative Diseases.

Annamaria Lanzillotta, Vanessa Porrini, Arianna Bellucci, Marina Benarese, Caterina Branca, Edoardo Parrella, Pier Franco Spano, Marina Pizzi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 91 citations in OpenAlex.

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  12. Involvement of KAntioxidants (Basel, Switzerland) · 2024
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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 2 institutions in 1 country.

Annamaria LanzillottaDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy.
Vanessa PorriniDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy ; IRCCS, San Camillo Hospital , Venice , Italy.
Arianna BellucciDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy.
Marina BenareseDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy.
Caterina BrancaDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy.
Edoardo ParrellaDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy.
Pier Franco SpanoDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy ; IRCCS, San Camillo Hospital , Venice , Italy.
Marina PizziDepartment of Molecular and Translational Medicine, National Institute of Neuroscience, University of Brescia , Brescia , Italy ; IRCCS, San Camillo Hospital , Venice , Italy.
University of Brescia · ITIRCCS San Camillo Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NF-κB factors are cardinal transcriptional regulators of inflammation and apoptosis, involved in the brain programing of systemic aging and in brain damage. The composition of NF-κB active dimers and epigenetic mechanisms modulating histone acetylation, finely condition neuronal resilience to brain insults. In stroke models, the activation of NF-κB/c-Rel promotes neuroprotective effects by transcription of specific anti-apoptotic genes. Conversely, aberrant activation of NF-κB/RelA showing reduced level of total acetylation, but site-specific acetylation on lysine 310, triggers the expression of pro-apoptotic genes. Constitutive knockout of c-Rel shatters the resilience of substantia nigra (SN) dopaminergic (DA) neurons to aging and induces a parkinsonian like pathology in mice. c-rel(-/-) mice show increased level of aberrantly acetylated RelA in the basal ganglia, neuroinflammation, accumulation of alpha-synuclein, and iron. Moreover, they develop motor deficits responsive to l-DOPA treatment and associated with loss of DA neurons in the SN. Here, we discuss the effect of unbalanced activation of RelA and c-Rel during aging and propose novel challenges for the development of therapeutic strategies in neurodegenerative diseases.

Indexed as

BDNFc-Rel deficient miceepigenetic drugsNF-κBRelA (K310)

Identifiers

PMID26042083
PMCPMC4438602
OpenAlexW1526979969

What OpenQuestion holds

Textmetadata
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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.