Evidence map›Paper›PMID 32526057›Full record

ReviewEuropean journal of neurology2020

Amyotrophic lateral sclerosis: a clinical review.

P Masrori, P Van Damme

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

Review in European journal of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 644 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
644citing papers in PubMed, 5 pooled it
39.9field-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.

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

644 citing papers in PubMed, 5 syntheses or guidelines pooled it, 1,111 citations in OpenAlex.

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  16. Potential Roles of Neuroimaging in Motor Neuron Disease.Current neurology and neuroscience reports · 2026
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584 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.

P MasroriDepartment of Neurosciences, Experimental Neurology, KU Leuven - University of Leuven, Leuven, Belgium.ORCID 0000-0001-8247-1866
P Van DammeDepartment of Neurosciences, Experimental Neurology, KU Leuven - University of Leuven, Leuven, Belgium.ORCID 0000-0002-4010-2357
VIB-KU Leuven Center for Brain & Disease Research · BE

Funding

'Een Hart voor ALSFlanders Innovation and Enterpreneurship (IWT grants Project MinE and iPSCAF)KU Leuven C1-C14-17-107Laeversfonds voor ALS OnderzoekOpening the Future Fund (KU Leuven)the ALS Liga Belgiumthe Alzheimer Research Foundation SAO-FRA 2017/023the Belgian National Lotterythe European Union's ERA-Net for Research Programmes on Rare Diseases (INTEGRALS)the European Union's Horizon 2020 research and innovation programme 755094the Flemish Government initiated Flanders Impulse Program on Networks for Dementia Research VIND 135043the Fund for Scientific Research Flanders (FWO-Flanders)the Latran FoundationValéry Perrier Race against ALS Fund
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting primarily the motor system, but in which extra-motor manifestations are increasingly recognized. The loss of upper and lower motor neurons in the motor cortex, the brain stem nuclei and the anterior horn of the spinal cord gives rise to progressive muscle weakness and wasting. ALS often has a focal onset but subsequently spreads to different body regions, where failure of respiratory muscles typically limits survival to 2-5 years after disease onset. In up to 50% of cases, there are extra-motor manifestations such as changes in behaviour, executive dysfunction and language problems. In 10%-15% of patients, these problems are severe enough to meet the clinical criteria of frontotemporal dementia (FTD). In 10% of ALS patients, the family history suggests an autosomal dominant inheritance pattern. The remaining 90% have no affected family members and are classified as sporadic ALS. The causes of ALS appear to be heterogeneous and are only partially understood. To date, more than 20 genes have been associated with ALS. The most common genetic cause is a hexanucleotide repeat expansion in the C9orf72 gene, responsible for 30%-50% of familial ALS and 7% of sporadic ALS. These expansions are also a frequent cause of frontotemporal dementia, emphasizing the molecular overlap between ALS and FTD. To this day there is no cure or effective treatment for ALS and the cornerstone of treatment remains multidisciplinary care, including nutritional and respiratory support and symptom management. In this review, different aspects of ALS are discussed, including epidemiology, aetiology, pathogenesis, clinical features, differential diagnosis, investigations, treatment and future prospects.

Indexed as

Amyotrophic Lateral SclerosisFrontotemporal DementiaC9orf72 ProteinDNA-Binding ProteinsHumansMotor NeuronsC9orf72 ProteinDNA-Binding Proteinsamyotrophic lateral sclerosissporadic and familial ALSTDP-43 pathology

Identifiers

PMID32526057
PMCPMC7540334
OpenAlexW3034958546

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.