Evidence map›Paper›PMID 24126629›Full record

ReviewNature reviews. Neurology2013

The epidemiology of ALS: a conspiracy of genes, environment and time.

Ammar Al-Chalabi, Orla Hardiman

Registry-linked trialOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02714036 (A Multi-Center, Open-Label Biomarker Study to Evaluate MN-166 in Subjects With Amyotrophic Literal Sclerosis), which is not on this map. Cited by 441 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
441citing papers in PubMed, 8 pooled it
29.0field-weighted citation impact, top 1% 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.

NCT02714036 phase1 / phase2completednot on this mapstarted 2016, after this paper: background citation

A Multi-Center, Open-Label Biomarker Study to Evaluate MN-166 in Subjects With Amyotrophic Literal Sclerosis (ALS)

TypeinterventionalSponsorMediciNovaRan2016 to 2020Enrolled35ConditionsAmyotrophic Lateral SclerosisArmsibudilast, Ibudilast
3 · Its place in the literature

Who cites it

441 citing papers in PubMed, 8 syntheses or guidelines pooled it, 870 citations in OpenAlex.

  1. Pooled it
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  4. The level of homocysteine in amyotrophic lateral sclerosis: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
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  7. A systematic review on the risk of neurodegenerative diseases and neurocognitive disorders in professional and varsity athletes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
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381 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

2 authors at 1 institution in 1 country.

Ammar Al-ChalabiKing's College London, Institute of Psychiatry, Department of Clinical Neuroscience, London SE5 8AF, UK.
Orla Hardiman
Trinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a relentlessly progressive neurodegenerative disease of motor neurons, resulting in worsening weakness of voluntary muscles until death from respiratory failure occurs after about 3 years. Although great advances have been made in our understanding of the genetic causes of ALS, the contribution of environmental factors has been more difficult to assess. Large-scale studies of the clinical patterns of ALS, individual histories preceding the onset of ALS, and the rates of ALS in different populations and groups have led to improved patient care, but have not yet revealed a replicable, definitive environmental risk factor. In this Review, we outline what is currently known of the environmental and genetic epidemiology of ALS, describe the current state of the art with respect to the different types of ALS, and explore whether ALS should be considered a single disease or a syndrome. We examine the relationship between genetic and environmental risk factors, and propose a disease model in which ALS is considered to be the result of environmental risks and time acting on a pre-existing genetic load, followed by an automatic, self-perpetuating decline to death.

Indexed as

Gene-Environment InteractionAmyotrophic Lateral SclerosisHumansRisk FactorsTime

Identifiers

PMID24126629
OpenAlexW2050626075

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.