Evidence map›Paper›PMID 32995988›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2021

DYNLT1 gene expression is downregulated in whole blood of patients at different Huntington's disease stages.

S M Rosseto, T A Alarcon, D M C Rocha, F M Ribeiro, S S G Ferguson, C Martins-Silva, M R Muniz, P F Costa, D A Guimarães, Rita G W Pires

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, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 53% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

10 authors at 4 institutions in 2 countries.

S M RossetoGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
T A AlarconLaboratory of Molecular and Behavioral Neurobiology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
D M C RochaDepartment of Pharmaceutical Sciences, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, 29043-900, Brazil.
F M RibeiroDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
S S G FergusonDepartment of Cellular and Molecular Medicine, Brain and Mind Research Institute and Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
C Martins-SilvaGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
M R MunizDepartment of Clinical Medicine, Health Science Center, Federal University of Espírito Santo, Espírito Santo, Brazil.
P F CostaDepartment of Physiotherapy, School of Sciences, Santa Casa de Misericordia de Vitoria, Vitória, ES, Brazil.
D A GuimarãesGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
Rita G W PiresGraduate Program in Biochemistry and Pharmacology, Health Sciences Center, Federal University of Espírito Santo, Vitória, ES, Brazil. rita.pires@ufes.br.ORCID http://orcid.org/0000-0002-4739-8349
Universidade Federal do Espírito Santo · BREscola Superior de Ciências da Santa Casa de Misericórdia de Vitória · BRUniversidade Federal de Minas Gerais · BRUniversity of Ottawa · CA

Funding

Fundação Estadual de Amparo à Pesquisa do Estado do Espírito Santo 65823648/2014.
6 · The paper itself

Abstract

Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG nucleotide expansion, which encodes the amino acid glutamine, in the huntingtin gene. HD is characterized by motor, cognitive, and psychiatric dysfunctions. In a previous study, we showed by qPCR that some genes altered in an HD mouse model were also altered in blood of HD patients. These alterations were mainly with respect to the dynein family. Therefore, this study aimed to investigate whether dynein light chain Tctex type 1 (DYNLT1) is altered in HD patients and if there is a correlation between DYNLT1 gene expression changes and disease progression. We assessed the DYNLT1 gene expression in the blood of 19 HD patients and 20 healthy age-matched controls. Also, in 6 of these patients, we analyzed the DYNLT1 expression at two time points, 3 years apart. The DYNLT1 gene expression in the whole blood of HD patients was significantly downregulated and this difference was widened in later stages. These data suggest that DYNLT1 could emerge as a peripheral prognostic indicator in HD and, also, might be a target for potential intervention in the future.

Indexed as

Huntington DiseaseAnimalsCase-Control StudiesDisease Models, AnimalDisease ProgressionDyneinsGene ExpressionHumansHuntingtin ProteinMiceDyneinsDYNLT1 protein, humanHuntingtin ProteinBiomarkerDYNLT1Gene expressionHuntington’s disease

Identifiers

PMID32995988
OpenAlexW3090525959

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.