Evidence map›Paper›PMID 32638105›Full record

ArticleJournal of neurology2020

Targeted next-generation sequencing study in familial ALS-FTD Portuguese patients negative for C9orf72 HRE.

Marta Gromicho, Ana Margarida Coutinho, Ana Catarina Pronto-Laborinho, Rita Raposeiro, Joana Tavares, Diana Antunes, Mamede de Carvalho

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurology, 2020. 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
0.3field-weighted citation impact, top 40% 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, 4 citations in OpenAlex.

  1. Genetic analysis ofFrontiers in aging neuroscience · 2025
    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

7 authors at 1 institution in 1 country.

Marta GromichoInstituto de Medicina Molecular and Institute of Physiology, Faculdade de Medicina da Universidade de Lisboa, Av. Professor Egas Moniz, 1648-028, Lisbon, Portugal. martalgms@gmail.com.ORCID http://orcid.org/0000-0003-2111-4579
Ana Margarida CoutinhoGenoMed-Diagnósticos de Medicina Molecular SA, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.
Ana Catarina Pronto-LaborinhoInstituto de Medicina Molecular and Institute of Physiology, Faculdade de Medicina da Universidade de Lisboa, Av. Professor Egas Moniz, 1648-028, Lisbon, Portugal.
Rita RaposeiroGenoMed-Diagnósticos de Medicina Molecular SA, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.
Joana TavaresGenoMed-Diagnósticos de Medicina Molecular SA, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.
Diana AntunesGenoMed-Diagnósticos de Medicina Molecular SA, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.
Mamede de CarvalhoInstituto de Medicina Molecular and Institute of Physiology, Faculdade de Medicina da Universidade de Lisboa, Av. Professor Egas Moniz, 1648-028, Lisbon, Portugal.
University of Lisbon · PT

Funding

Fundação para a Ciência e a Tecnologia PTDC/MEC-NEU/31195/2017
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease with clinical and etiological heterogeneity and a complex genetic contribution. Clinical, neuropathological, and genetic evidence revealed that ALS and frontotemporal dementia (FTD) are in part of a single disease continuum. Genetic causes have been identified in sporadic (SALS) and familial patients (FALS) and the recurrent genetic factor underlying ALS and FTD is the C9orf72 hexanucleotide repeat expansion (HRE). However, in our population, the concomitance of ALS and FTD cannot be explained by C9orf72 HRE in many FALS and SALS cases. Our aim is to further understand the genetic basis of ALS in Portuguese patients. 34 patients with FALS or SALS-FTD, negative for C9orf72 HRE, were screened for rare variants in a panel of 29 relevant genes by next-generation sequencing. We detected 15 variants in 11 genes, one classified as pathogenic in TARDBP, two as likely pathogenic in TARDBP and PRPH, and the others as variants of unknown significance (VUS). Gene variants, including VUS, were found in 41.2% FALS patients and 40% SALS-FTD. In most patients, no potential pathogenic variants were found. Our results emphasize the need to enhance the efforts to unravel the genetic architecture of ALS-FTD.

Indexed as

Amyotrophic Lateral SclerosisFrontotemporal DementiaNeurodegenerative DiseasesC9orf72 ProteinDNA Repeat ExpansionHigh-Throughput Nucleotide SequencingHumansPortugalC9orf72 ProteinC9orf72 protein, humanAmyotrophic lateral sclerosisFrontotemporal dementiaGenetic screeningGene variantsNext-generation sequencing

Identifiers

PMID32638105
OpenAlexW3040865524

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.