Evidence map›Paper›PMID 35481544›Full record

ArticleBrain : a journal of neurology2023

Mosaic divergent repeat interruptions in XDP influence repeat stability and disease onset.

Joanne Trinh, Theresa Lüth, Susen Schaake, Björn-Hergen Laabs, Kathleen Schlüter, Joshua Laβ, Jelena Pozojevic, Ronnie Tse, Inke König, Roland Dominic Jamora and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Alterations in energy production in aFrontiers in aging neuroscience · 2026
    Article
  4. Integrating Long-Read Nanopore Sequencing for Precision Resolution of Genomic Variants in Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  5. Article
  6. Long-Read Sequencing: The Third Generation of Diagnostic Testing for Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2025
    Review
  7. Exploration of Neurodegenerative Diseases Using Long-Read Sequencing and Optical Genome Mapping Technologies.Movement disorders : official journal of the Movement Disorder Society · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Genetic Testing of Movements Disorders: A Review of Clinical Utility.Tremor and other hyperkinetic movements (New York, N.Y.) · 2024
    Review
  14. Article
  15. Article
  16. Parkinson's Disease is Predominantly a Genetic Disease.Journal of Parkinson's disease · 2024
    Review
  17. Review
  18. Article
  19. 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

19 authors at 8 institutions in 4 countries.

Joanne TrinhInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.ORCID 0000-0001-5317-7369
Theresa LüthInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Susen SchaakeInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Björn-Hergen LaabsInstitute of Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
Kathleen SchlüterInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Joshua LaβInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Jelena PozojevicInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Ronnie TseInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Inke KönigInstitute of Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
Roland Dominic JamoraDepartment of Neurosciences, College of Medicine-Philippine General Hospital, University of the Philippines Manila, Manila, Philippines.
Raymond L RosalesDepartment of Neurology and Psychiatry, University of Santo Tomas and the CNS-Metropolitan Medical Center, Manila, Philippines.ORCID 0000-0001-6387-1389
Norbert BrüggemannInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.ORCID 0000-0001-5969-6899
Gerard SaranzaSection of Neurology, Department of Internal Medicine, Chong Hua Hospital, Cebu, Philippines.ORCID 0000-0001-8322-4226
Cid Czarina E DiestaDepartment of Neurosciences, Movement Disorders Clinic, Makati Medical Center, Makati City, Philippines.
Frank J KaiserInstitute for Human Genetics at the University Hospital Essen, Essen, Germany.
Christel DepienneInstitute for Human Genetics at the University Hospital Essen, Essen, Germany.
Christopher E PearsonProgram of Genetics and Genome Biology, The Hospital for Sick Children, The Peter Gilgan Centre for Research and Learning, Toronto, Canada.
Ana WestenbergerInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Christine KleinInstitute of Neurogenetics, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
University Hospital Schleswig-Holstein · DEEssen University Hospital · DEUniversity of Lübeck · DEChang Hua Hospital · TWMakati Medical Center · PHPhilippine General Hospital · PHUniversity of Santo Tomas · PHUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While many genetic causes of movement disorders have been identified, modifiers of disease expression are largely unknown. X-linked dystonia-parkinsonism (XDP) is a neurodegenerative disease caused by a SINE-VNTR-Alu(AGAGGG)n retrotransposon insertion in TAF1, with a polymorphic (AGAGGG)n repeat. Repeat length and variants in MSH3 and PMS2 explain ∼65% of the variance in age at onset (AAO) in XDP. However, additional genetic modifiers are conceivably at play in XDP, such as repeat interruptions. Long-read nanopore sequencing of PCR amplicons from XDP patients (n = 202) was performed to assess potential repeat interruption and instability. Repeat-primed PCR and Cas9-mediated targeted enrichment confirmed the presence of identified divergent repeat motifs. In addition to the canonical pure SINE-VNTR-Alu-5'-(AGAGGG)n, we observed a mosaic of divergent repeat motifs that polarized at the beginning of the tract, where the divergent repeat interruptions varied in motif length by having one, two, or three nucleotides fewer than the hexameric motif, distinct from interruptions in other disease-associated repeats, which match the lengths of the canonical motifs. All divergent configurations occurred mosaically and in two investigated brain regions (basal ganglia, cerebellum) and in blood-derived DNA from the same patient. The most common divergent interruption was AGG [5'-SINE-VNTR-Alu(AGAGGG)2AGG(AGAGGG)n], similar to the pure tract, followed by AGGG [5'-SINE-VNTR-Alu(AGAGGG)2AGGG(AGAGGG)n], at median frequencies of 0.425 (IQR: 0.42-0.43) and 0.128 (IQR: 0.12-0.13), respectively. The mosaic AGG motif was not associated with repeat number (estimate = -3.8342, P = 0.869). The mosaic pure tract frequency was associated with repeat number (estimate = 45.32, P = 0.0441) but not AAO (estimate = -41.486, P = 0.378). Importantly, the mosaic frequency of the AGGG negatively correlated with repeat number after adjusting for age at sampling (estimate = -161.09, P = 3.44 × 10-5). When including the XDP-relevant MSH3/PMS2 modifier single nucleotide polymorphisms into the model, the mosaic AGGG frequency was associated with AAO (estimate = 155.1063, P = 0.047); however, the association dissipated after including the repeat number (estimate = -92.46430, P = 0.079). We reveal novel mosaic divergent repeat interruptions affecting both motif length and sequence (DRILS) of the canonical motif polarized within the SINE-VNTR-Alu(AGAGGG)n repeat. Our study illustrates: (i) the importance of somatic mosaic genotypes; (ii) the biological plausibility of multiple modifiers (both germline and somatic) that can have additive effects on repeat instability; and (iii) that these variations may remain undetected without assessment of single molecules.

Indexed as

Dystonic DisordersGenetic Diseases, X-LinkedNeurodegenerative DiseasesHumansMismatch Repair Endonuclease PMS2Mismatch Repair Endonuclease PMS2genetic modifiers‌mosaicrepeat interruptionssingle-molecule sequencingX-linked dystonia parkinsonism

Identifiers

PMID35481544
PMCPMC9976955
OpenAlexW4225105043

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.