Evidence map›Paper›PMID 38320749›Full record

ArticleLipids2024

Alteration of serum bile acids in amyotrophic lateral sclerosis.

Ikjae Lee, Renu Nandakumar, Rebecca A Haeusler

Open access · greenAbstract read
In one paragraph

Article in Lipids, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Emerging Roles of Bile Acids in Neuroinflammation.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Review
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

3 authors at 2 institutions in 1 country.

Ikjae LeeDepartment of Neurology, Columbia University, New York, New York, USA.
Renu NandakumarBiomarkers Core Laboratory, Irving Institute for Clinical and Translational Research, Columbia University Irving Medical Center, New York, New York, USA.
Rebecca A HaeuslerDepartment of Pathology & Cell Biology and Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA.
Columbia University · USColumbia University Irving Medical Center · US

Funding

Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
Bile acids and insulin sensitivityR01DK115825 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Rebecca Anne Haeusler · 2018 to 2026
$5.4M
Metabolic Alteration in Presymptomatic and Symptomatic ALS Study (MAPS ALS Study)K23NS131586 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Ikjae Lee · 2023 to 2026
$919k
American Academy of NeurologyAmerican Brain FoundationNational Center for Advancing Translational Sciences, National Institutes of Health ULTR001873NIDDK NIH HHS R01 DK115825NIH HHS K23NS131586NIH HHS R01DK115825NINDS NIH HHS K23 NS131586
6 · The paper itself

Abstract

Hydrophilic endogenous bile acids ursodeoxycholic acid (UDCA), tauroursodeoxycholic acid (TUDCA), and glucourosodeoxycholic acid (GUDCA) have suggested neuroprotective effects. We performed a case-control study to examine the association between ALS diagnosis and serum levels of bile acids. Sporadic and familial ALS patients, age- and sex-matched healthy controls, and presymptomatic gene carriers who donated blood samples were included. Non-fasted serum samples stored at -80°C were used for the analysis. Serum bile acid levels were measured by liquid chromatography-mass spectrometry (LC-MS). Concentrations of 15 bile acids were obtained, 5 non-conjugated and 10 conjugated, and compared between ALS versus control groups (presymptomatic gene carriers + healthy controls) using the Wilcoxon-Rank-Sum test. In total, 80 participants were included: 31 ALS (17 sporadic and 14 familial ALS); 49 controls (22 gene carriers, 27 healthy controls). The mean age was 50 years old and 50% were male. In the ALS group, 45% had familial disease with a pathogenic variant in C9orf72 (29%), TARDBP (10%), FUS (3%), and CHCHD10 (3%) genes. In the control group, 43% carried pathogenic variants: C9orf72 (27%), SOD1 (10%), and FUS (6%). The serum levels of UDCA, TUDCA, and GUDCA trended higher in the ALS group compared to controls (median 27 vs. 7 nM, 4 vs. 3 nM, 110 vs. 47 nM, p-values 0.04, 0.06, 0.04, respectively). No significant group differences were found in other bile acids serum levels. In conclusion, the serum level of UDCA, TUDCA, GUDCA trended higher in ALS patients compared to controls, and no evidence of deficiencies was found.

Indexed as

Amyotrophic Lateral SclerosisBile Acids and SaltsAdultAgedCase-Control StudiesFemaleHumansMaleMiddle AgedBile Acids and Saltsamyotrophic lateral sclerosisbile acidsmetabolismpathogenic variant carriertaursourodeoxycholic acidTUDCA

Identifiers

PMID38320749
PMCPMC11226384
OpenAlexW4391630427

What OpenQuestion holds

Textmetadata
LicenceTDM
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.