Evidence map›Paper›PMID 25119539›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2015

Common mechanisms in neurodegeneration and neuroinflammation: a BrainNet Europe gene expression microarray study.

Pascal F Durrenberger, Francesca S Fernando, Samira N Kashefi, Tim P Bonnert, Danielle Seilhean, Brahim Nait-Oumesmar, Andrea Schmitt, Peter J Gebicke-Haerter, Peter Falkai, Edna Grünblatt and 5 more

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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 8 pooled it
–field-weighted citation impact
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

79 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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  19. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
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19 more citing papers are in PubMed but not listed here.

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

15 authors.

Pascal F DurrenbergerWolfson Neuroscience Laboratories, Division of Brain Sciences, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Burlington Danes Building, Du Cane Road, London, W12 0NN, UK.
Francesca S Fernando
Samira N Kashefi
Tim P Bonnert
Danielle Seilhean
Brahim Nait-Oumesmar
Andrea Schmitt
Peter J Gebicke-Haerter
Peter Falkai
Edna Grünblatt
Miklos Palkovits
Thomas Arzberger
Hans Kretzschmar
David T Dexter
Richard Reynolds

Funding

Parkinson's UK G-0909
6 · The paper itself

Abstract

Neurodegenerative diseases of the central nervous system are characterized by pathogenetic cellular and molecular changes in specific areas of the brain that lead to the dysfunction and/or loss of explicit neuronal populations. Despite exhibiting different clinical profiles and selective neuronal loss, common features such as abnormal protein deposition, dysfunctional cellular transport, mitochondrial deficits, glutamate excitotoxicity, iron accumulation and inflammation are observed in many neurodegenerative disorders, suggesting converging pathways of neurodegeneration. We have generated comparative genome-wide gene expression data, using the Illumina HumanRef 8 Beadchip, for Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis, Parkinson's disease, and schizophrenia using an extensive cohort (n = 113) of well-characterized post-mortem brain tissues. The analysis of whole-genome expression patterns across these major disorders offers an outstanding opportunity not only to look into exclusive disease-specific changes, but more importantly to look for potential common molecular pathogenic mechanisms. Surprisingly, no dysregulated gene that passed our selection criteria was found in common across all six diseases. However, 61 dysregulated genes were shared when comparing five and four diseases. The few genes highlighted by our direct gene comparison analysis hint toward common neuronal homeostatic, survival and synaptic plasticity pathways. In addition, we report changes to several inflammation-related genes in all diseases. This work is supportive of a general role of the innate immune system in the pathogenesis and/or response to neurodegeneration.

Indexed as

AdultAgedAged, 80 and overBrainCohort StudiesEncephalitisEuropeFemaleGene ExpressionHumansMaleMicroarray AnalysisMiddle AgedNeurodegenerative DiseasesNeurogliaPrincipal Component AnalysisRNA, Messenger

Identifiers

PMID25119539

What OpenQuestion holds

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Registered trials

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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.