Evidence map›Paper›PMID 20232219›Full record

ArticleNeurogenetics2010

L239F founder mutation in GDAP1 is associated with a mild Charcot-Marie-Tooth type 4C4 (CMT4C4) phenotype.

Dagmara Kabzińska, Halina Strugalska-Cynowska, Anna Kostera-Pruszczyk, Barbara Ryniewicz, Renata Posmyk, Alina Midro, Pavel Seeman, Lucia Báranková, Magdalena Zimoń, Jonathan Baets and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurogenetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Homozygous Mutations inDNA and cell biology · 2023
    Article
  3. Article
  4. Mutations inInternational journal of molecular sciences · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. 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

18 authors at 9 institutions in 4 countries.

Dagmara KabzińskaMossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Halina Strugalska-Cynowska
Anna Kostera-Pruszczyk
Barbara Ryniewicz
Renata Posmyk
Alina Midro
Pavel Seeman
Lucia Báranková
Magdalena Zimoń
Jonathan Baets
Vincent Timmerman
Velina Guergueltcheva
Ivailo Tournev
Stayko Sarafov
Peter De Jonghe
Albena Jordanova
Irena Hausmanowa-Petrusewicz
Andrzej Kochański
Medical University of Sofia · BGMossakowski Medical Research Institute, Polish Academy of Sciences · PLUniversity of Antwerp · BECharles University · CZMedical University of Białystok · PLMedical University of Warsaw · PLAntwerp University Hospital · BEPolish Academy of Sciences · PLVIB-UAntwerp Center for Molecular Neurology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over 40 mutations in the GDAP1 gene have been shown to segregate with Charcot-Marie-Tooth disease (CMT). Among these, only two mutations, i.e., S194X and Q163X have been reported in a sufficient number of CMT families to allow for the construction of reliable phenotype-genotype correlations. Both the S194X and Q163X mutations have been shown to segregate with an early-onset and severe neuropathy resulting in loss of ambulance at the beginning of the second decade of life. In this study, we identified the L239F mutation in the GDAP1 gene in one Bulgarian and five Polish families. We hypothesized that the L239F mutation may result from a founder effect in the European population since this mutation has previously been reported in Belgian, Czech, and Polish patients. In fact, we detected a common disease-associated haplotype within the 8q13-q21 region in the Polish, German, Italian, Czech, and Bulgarian CMT families. Like the previously detected "regional" S194X and Q163X mutations, respectively present in Maghreb countries and in patients of Spanish descent, the L239F mutation seems to be the most common GDAP1 pathogenic variant in the Central and Eastern European population. Given the likely presence of a common ancestor harboring the L239F mutation, we decided to compare the phenotypes of the CMT (L239F) patients collected in this study with those of previously reported cases. In contrast to CMT4A caused by the S194X and Q163X mutations, the CMT phenotype resulting from the L239F substitution represents a milder clinical entity with a long-preserved period of ambulance at least until the end of the second decade of life.

Indexed as

Founder EffectAdolescentAdultAge of OnsetCharcot-Marie-Tooth DiseaseChildChild, PreschoolChromosomes, Human, Pair 8EuropeFemaleGenetic Association StudiesGenetic LociHumansIntracellular Signaling Peptides and ProteinsMaleMutationGDAP proteinIntracellular Signaling Peptides and ProteinsNerve Tissue ProteinsProteinsSH3TC2 protein, human

Identifiers

PMID20232219
OpenAlexW2093420579

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.