Evidence map›Paper›PMID 31000966›Full record

ArticleAnnals of neurosciences2018

Gene-Environment-Time Interactions in Neurodegenerative Diseases: Hypotheses and Research Approaches.

Walter G Bradley, Angeline S Andrew, Bryan J Traynor, Adriano Chiò, Tanya H Butt, Elijah W Stommel

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

Article in Annals of neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. 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
    Pooled it
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  7. Genetics of Hypertension: From Monogenic Analysis to GETomics.Journal of cardiovascular development and disease · 2024
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  20. Destination Amyotrophic Lateral Sclerosis.Frontiers in neurology · 2021
    Article
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

6 authors at 4 institutions in 2 countries.

Walter G BradleyDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, Florida, USA.
Angeline S AndrewDepartment of Neurology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA.
Bryan J TraynorNeuromuscular Diseases Research Section, Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, Maryland, USA.
Adriano Chiò"Rita Levi Montalcini" Department of Neuroscience, University of Turin, Turin, Italy.
Tanya H ButtDepartment of Neurology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA.
Elijah W StommelDepartment of Neurology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA.
Dartmouth College · USNational Institutes of Health · USUniversity of Miami · USUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmyotrophic lateral sclerosis (ALS), Alzheimer's, and Parkinson's diseases are age-related neurodegenerative diseases. ALS is not a single entity but a syndrome with many different causes. In all 3 diseases, gene mutations account for only 10-15% of cases. Many environmental and lifestyle factors have been implicated as risk factors for ALS, though none have been proven to cause the disease. It is generally believed that ALS results from interactions between environmental risk factors and genetic predisposing factors. The advent of next-generation sequencing and recent advances in research into environmental risk factors offer the opportunity to investigate these interactions. SUMMARY: We propose a hypothesis to explain the syndrome of ALS based on the interaction of many individual environmental risk factors with many individual genetic predisposing factors. We hypothesize that there are many such combinations of individual, specific, genetic, and environmental factors, and that each combination can lead to the development of the syndrome of ALS. We also propose a hypothesis that explains the overlap between the age-related neurodegenerations and their genetic underpinnings. Age and duration of exposure are crucial factors in these age-related neurodegenerative diseases, and we consider how these may relate to gene-environment interactions. KEY MESSAGES: To date, genetic studies and environmental studies have investigated the causes of ALS separately. We argue that this univariate approach will not lead to discoveries of important gene-environment interactions. We propose new research approaches to investigating gene-environment interactions based on these hypotheses.

Indexed as

Amyotrophic lateral sclerosisEnvironmental risk factorsGene-environment-time interactionsGenetic predispositionNeurodegenerative diseases

Identifiers

PMID31000966
PMCPMC6470336
OpenAlexW2902229478

What OpenQuestion holds

Textmetadata
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.