Evidence map›Paper›PMID 33103324›Full record

ArticleHuman brain mapping2021

Disease aggressiveness signatures of amyotrophic lateral sclerosis in white matter tracts revealed by the D50 disease progression model.

Robert Steinbach, Nayana Gaur, Annekathrin Roediger, Thomas E Mayer, Otto W Witte, Tino Prell, Julian Grosskreutz

Open access · goldAbstract read
In one paragraph

Article in Human brain mapping, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Robert SteinbachHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.ORCID 0000-0003-3936-6010
Nayana GaurHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.ORCID 0000-0001-7854-6247
Annekathrin RoedigerHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Thomas E MayerDepartment of Neuroradiology, Jena University Hospital, Jena, Germany.
Otto W WitteHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.ORCID 0000-0003-2101-4105
Tino PrellHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.ORCID 0000-0002-6423-3108
Julian GrosskreutzHans Berger Department of Neurology, Jena University Hospital, Jena, Germany.ORCID 0000-0001-9525-1424
Jena University Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous neuroimaging studies in amyotrophic lateral sclerosis (ALS) have reported links between structural changes and clinical data; however phenotypic and disease course heterogeneity have occluded robust associations. The present study used the novel D50 model, which distinguishes between disease accumulation and aggressiveness, to probe correlations with measures of diffusion tensor imaging (DTI). DTI scans of 145 ALS patients and 69 controls were analyzed using tract-based-spatial-statistics of fractional anisotropy (FA), mean- (MD), radial (RD), and axial diffusivity (AD) maps. Intergroup contrasts were calculated between patients and controls, and between ALS subgroups: based on (a) the individual disease covered (Phase I vs. II) or b) patients' disease aggressiveness (D50 value). Regression analyses were used to probe correlations with model-derived parameters. Case-control comparisons revealed widespread ALS-related white matter pathology with decreased FA and increased MD/RD. These affected pathways showed also correlations with the accumulated disease for increased MD/RD, driven by the subgroup of Phase I patients. No significant differences were noted between patients in Phase I and II for any of the contrasts. Patients with high disease aggressiveness (D50 < 30 months) displayed increased AD/MD in bifrontal and biparietal pathways, which was corroborated by significant voxel-wise regressions with D50. Application of the D50 model revealed associations between DTI measures and ALS pathology in Phase I, representing individual disease accumulation early in disease. Patients' overall disease aggressiveness correlated robustly with the extent of DTI changes. We recommend the D50 model for studies developing/validating neuroimaging or other biomarkers for ALS.

Indexed as

Diffusion Tensor ImagingDisease ProgressionModels, NeurologicalAdultAgedAged, 80 and overAmyotrophic Lateral SclerosisFemaleHumansMaleMiddle AgedWhite Matteramyotrophic lateral sclerosisD50 modeldiffusion tensor imagingdisease aggressivenessdisease progressionTBSS

Identifiers

PMID33103324
PMCPMC7814763
OpenAlexW3093711584

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.