Evidence map›Paper›PMID 29907907›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2018

Three novel mutations in 20 patients with hereditary spastic paraparesis.

Mehmet Bugrahan Duz, Selcuk Dasdemir, Aysel Kalayci Yigin, Mehmet Ali Akalin, Mehmet Seven

Abstract read
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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 59% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. NovelWorld journal of clinical cases · 2019
    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

5 authors at 1 institution in 1 country.

Mehmet Bugrahan DuzDepartment of Medical Genetics, Cerrahpaşa Medical School, Istanbul University-Cerrahpaşa, 34098, Fatih, Istanbul, Turkey.
Selcuk DasdemirDepartment of Medical Genetics, Cerrahpaşa Medical School, Istanbul University-Cerrahpaşa, 34098, Fatih, Istanbul, Turkey.
Aysel Kalayci YiginDepartment of Medical Genetics, Cerrahpaşa Medical School, Istanbul University-Cerrahpaşa, 34098, Fatih, Istanbul, Turkey.
Mehmet Ali AkalinDepartment of Neurology, Cerrahpaşa Medical School, Istanbul University-Cerrahpaşa, 34098, Fatih, Istanbul, Turkey.
Mehmet SevenDepartment of Medical Genetics, Cerrahpaşa Medical School, Istanbul University-Cerrahpaşa, 34098, Fatih, Istanbul, Turkey. mimseven@istanbul.edu.tr.ORCID http://orcid.org/0000-0001-7878-2039
Istanbul University-Cerrahpaşa · TR

Funding

Bilimsel Araştirma Projeleri Birimi, Istanbul Üniversitesi 22323
6 · The paper itself

Abstract

Hereditary spastic paraparesis (HSP) constitutes both genetic and clinically heterogeneous group of upper motor neuron diseases. Half of the individuals with autosomal dominant (AD) HSP have mutations in SPAST, ATL1, and REEP1 genes. This study was conducted to elucidate the genetic etiology of patients with the pure type AD-HSP diagnosis. The patient group consisted of 23 individuals from 6 families in Turkey. In the first step of work, Sanger sequencing (SS) was performed in ATL1, SPAST, and REEP1 genes and the second phase whole-exome sequencing (WES) was performed following SS analysis for the patients with no detected mutations in these genes. The results of this study revealed that in ATL1, 6 patients have previously reported c.776C > A mutation and 6 patients have novel c.470 T > C mutation. In SPAST, 3 patients have novel c.1072G > C mutation and 2 patients have novel c.1099-1G > C mutation. WES was performed in three patients, who had no detected mutation in these genes with SS analysis. In this approach, as previously reported c.1859 T > C mutation in KIAA0196 was detected, and it was confirmed with the patient's relatives by SS. In three of patients, no HSP-associated variant could be identified in SS and WES. With this study, the molecular genetic etiology in 20 of 23 (87%) individuals that were included in this study with the utilization of SS and WES was elucidated. Utilization of SS and WES methods have enabled the identification of genetic etiology of HSP further with appropriate genetic counseling that was provided to the patients.

Indexed as

Genetic Predisposition to DiseaseMutationAdolescentAdultAgedChildCohort StudiesExome SequencingFamilyFemaleGenes, DominantGenetic Association StudiesGTP-Binding ProteinsHumansMaleMembrane ProteinsATL1 protein, humanGTP-Binding ProteinsMembrane ProteinsMembrane Transport ProteinsProteinsREEP1 protein, humanSpastinSPAST protein, humanWASHC5 protein, humanGenetic heterogeneityHereditary spastic paraparesisNovel mutationWhole-exome sequencing

Identifiers

PMID29907907
OpenAlexW2807917203

What OpenQuestion holds

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Registered trials

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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.