Evidence map›Paper›PMID 30220791›Full record

ReviewMedizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V2018

Current knowledge and recent insights into the genetic basis of amyotrophic lateral sclerosis.

Alexander E Volk, Jochen H Weishaupt, Peter M Andersen, Albert C Ludolph, Christian Kubisch

Open access · hybridAbstract readReview
In one paragraph

Review in Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
13.3field-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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Human tissue lead (Pb) levels and amyotrophic lateral sclerosis: a systematic review and meta-analysis of case-control studies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Pooled it
  3. Synaptic Proteostasis in Health and Disease.Journal of neurochemistry · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Myofiber Type Shift in Extraocular Muscles in Amyotrophic Lateral Sclerosis.Investigative ophthalmology & visual science · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

4 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

5 authors at 3 institutions in 2 countries.

Alexander E Volk1Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Jochen H Weishaupt2Department of Neurology, Ulm University, Ulm, Germany.
Peter M Andersen2Department of Neurology, Ulm University, Ulm, Germany.
Albert C Ludolph2Department of Neurology, Ulm University, Ulm, Germany.
Christian Kubisch1Institute of Human Genetics, University Medical Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Universität Ulm · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is the most frequent motor neuron disease, affecting the upper and/or lower motor neurons. However, extramotor symptoms can also occur; cognitive deficits are present in more than 40% of patients and 5-8% of ALS patients develop frontotemporal dementia. There is no effective treatment for ALS and median survival is 2-3 years after onset. Amyotrophic lateral sclerosis is a genetically heterogeneous disorder with monogenic forms as well as complex genetic etiology. Currently, complex genetic risk factors are of minor interest for routine diagnostic testing or counseling of patients and their families. By contrast, a monogenic cause can be identified in 70% of familial and 10% of sporadic ALS cases. The most frequent genetic cause is a noncoding hexanucleotide repeat expansion in the

Indexed as

C9orf72Genetic heterogeneityMotor neuron diseaseOligogenic inheritancePredictive testing

Identifiers

PMID30220791
PMCPMC6132774
OpenAlexW2883160990

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.