Evidence map›Paper›PMID 37543248›Full record

ArticleBrain, behavior, and immunity2023

Systemic inflammation and subsequent risk of amyotrophic lateral sclerosis: Prospective cohort study.

G David Batty, Mika Kivimäki, Philipp Frank, Catharine R Gale, Liam Wright

Open access · hybridAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

G David BattyDepartment of Epidemiology and Public Health, University College London, UK. Electronic address: david.batty@ucl.ac.uk.
Mika KivimäkiUCL Brain Sciences, University College London, UK; Clinicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland. Electronic address: mika.kivimaki@helsinki.fi.
Philipp FrankDepartment of Epidemiology and Public Health, University College London, UK. Electronic address: philipp.frank.16@ucl.ac.uk.
Catharine R GaleMRC Lifecourse Epidemiology Unit, University of Southampton, UK; Lothian Birth Cohorts, Department of Psychology, University of Edinburgh, UK. Electronic address: crg@mrc.soton.ac.uk.
Liam WrightCentre for Longitudinal Studies, University College London, UK. Electronic address: liam.wright@ucl.ac.uk.
University College London · GBNHS Lothian · GBUniversity of Helsinki · FI

Funding

Medical Research Council MR/P023444/1Medical Research Council MR/S011676/1
6 · The paper itself

Abstract

backgroundWhile systemic inflammation has been implicated in the etiology of selected neurodegenerative disorders, its role in the development of amyotrophic lateral sclerosis (ALS), a condition with high case-fatality, is untested. Accordingly, we quantified the relationship of C-reactive protein (CRP), an acute-phase reactant and marker of systemic inflammation, with subsequent ALS occurrence.

methodsWe used data from UK Biobank, a prospective cohort study of 502,649 participants who were aged 37 to 73 years when examined at research centers between 2006 and 2010. Venous blood was collected at baseline in the full cohort and assayed for CRP, and repeat measurement was made 3-7 years later in a representative subgroup (N = 14,514) enabling correction for regression dilution. ALS was ascertained via national hospitalization and mortality registries until 2021. We computed multivariable hazard ratios with accompanying 95% confidence intervals for log-transformed CRP expressed as standard deviation and tertiles.

resultsIn an analytical sample of 400,884 initially ALS-free individuals (218,203 women), a mean follow-up of 12 years gave rise to 231 hospitalizations and 223 deaths ascribed to ALS. After adjustment for covariates which included health behaviors, comorbidity, and socio-economic status, a one standard deviation higher log-CRP was associated with elevated rates of both ALS mortality (hazard ratios; 95% confidence intervals: 1.32; 1.13, 1.53) and hospitalizations (1.20; 1.00, 1.39). There was evidence of dose-response effects across tertiles of CRP for both outcomes (p for trend ≤ 0.05). Correction for regression dilution led to a strengthening of the relationship with CRP for both mortality (1.62; 1.27, 2.08) and hospitalizations (1.37; 1.05, 1.76).

conclusionsHigher levels of CRP, a blood-based biomarker widely captured in clinical practice, is associated with moderately increased future risk of amyotrophic lateral sclerosis.

Indexed as

Amyotrophic Lateral SclerosisBiomarkersC-Reactive ProteinFemaleHumansInflammationProspective StudiesBiomarkersC-Reactive Protein

Identifiers

PMID37543248
PMCPMC10937260
OpenAlexW4385597446

What OpenQuestion holds

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LicenceCC BY
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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.