Evidence map›Paper›PMID 19076696›Full record

ReviewNeuropathology and applied neurobiology2008

Review: Mitochondria and disease progression in multiple sclerosis.

D Mahad, H Lassmann, D Turnbull

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuropathology and applied neurobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

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30 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

3 authors at 2 institutions in 2 countries.

D MahadThe Mitochondrial Research Group, University of Newcastle upon Tyne, Newcastle, UK. d.j.mahad@ncl.ac.uk
H Lassmann
D Turnbull
Wellcome Centre for Mitochondrial Research · GBMedical University of Vienna · AT

Funding

Austrian Science Fund FWF P 19854Wellcome Trust
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. Recent evidence suggests that dysfunction of surviving demyelinated axons and axonal degeneration contribute to the progression of MS. We review the evidence for and potential mechanisms of degeneration as well as dysfunction of chronically demyelinated axons in MS with particular reference to mitochondria, the main source of adenosine-5'-triphosphate in axons. Besides adenosine-5'-triphosphate production, mitochondria play an important role in calcium handling and produce reactive oxygen species. The mitochondrial changes in axons lacking healthy myelin sheaths as well as redistribution of sodium channels suggest that demyelinated axons would be more vulnerable to energy deficit than myelinated axons. A dysfunction of mitochondria in lesions as well as in the normal-appearing white and grey matter is increasingly recognized in MS and could be an important determinant of axonal dysfunction and degeneration. Mitochondria are a potential therapeutic target in MS.

Indexed as

Adenosine TriphosphateAnimalsAxonsDemyelinating DiseasesDisease ProgressionEnergy MetabolismHumansMitochondriaMultiple SclerosisMyelin SheathNerve DegenerationAdenosine Triphosphate

Identifiers

PMID19076696
PMCPMC2981078
OpenAlexW2015016389

What OpenQuestion holds

Textmetadata
LicenceTDM
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.