Evidence map›Paper›PMID 32466798›Full record

ArticleBMC biology2020

Deficits in coordinated neuronal activity and network topology are striatal hallmarks in Huntington's disease.

S Fernández-García, J G Orlandi, G A García-Díaz Barriga, M J Rodríguez, M Masana, J Soriano, J Alberch

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

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  9. Unraveling the Spatiotemporal Distribution of VPS13A in the Mouse Brain.International journal of molecular sciences · 2021
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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

7 authors at 3 institutions in 2 countries.

S Fernández-GarcíaDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociències, Universitat de Barcelona, 08036, Barcelona, Spain.
J G OrlandiComplexity Science Group, Department of Physics and Astronomy, Faculty of Science, University of Calgary, Calgary, AB, T2N 1N4, Canada.
G A García-Díaz BarrigaDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociències, Universitat de Barcelona, 08036, Barcelona, Spain.
M J RodríguezDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociències, Universitat de Barcelona, 08036, Barcelona, Spain.
M MasanaDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociències, Universitat de Barcelona, 08036, Barcelona, Spain.
J SorianoDepartament de Física de la Matèria Condensada, Universitat de Barcelona, 08028, Barcelona, Spain.
J AlberchDepartament de Biomedicina, Facultat de Medicina, Institut de Neurociències, Universitat de Barcelona, 08036, Barcelona, Spain. alberch@ub.edu.ORCID 0000-0002-8684-2721
Biomedical Research Networking Center on Neurodegenerative Diseases · ESUniversitat de Barcelona · ESUniversity of Calgary · CA

Funding

Generalitat de Catalunya 2017-SGR-1061Horizon 2020 Framework Programme 713140Horizon 2020 Framework Programme 863214Instituto de Salud Carlos III RD06/0010/0006Ministerio de Ciencia, Innovación y Universidades FIS2016-78507-C2-2-PMinisterio de Ciencia, Innovación y Universidades FIS2017-90782-REDTMinisterio de Ciencia, Innovación y Universidades SAF2017-88076-R
6 · The paper itself

Abstract

backgroundNetwork alterations underlying neurodegenerative diseases often precede symptoms and functional deficits. Thus, their early identification is central for improved prognosis. In Huntington's disease (HD), the cortico-striatal networks, involved in motor function processing, are the most compromised neural substrate. However, whether the network alterations are intrinsic of the striatum or the cortex is not fully understood.

resultsIn order to identify early HD neural deficits, we characterized neuronal ensemble calcium activity and network topology of HD striatal and cortical cultures. We used large-scale calcium imaging combined with activity-based network inference analysis. We extracted collective activity events and inferred the topology of the neuronal network in cortical and striatal primary cultures from wild-type and R6/1 mouse model of HD. Striatal, but not cortical, HD networks displayed lower activity and a lessened ability to integrate information. GABA

conclusionsOverall, our integrative approach highlights striatal defective network integration capacity as a major contributor of basal ganglia dysfunction in HD and suggests that increased excitatory drive may serve as a potential intervention. In addition, our work provides a valuable tool to evaluate in vitro network recovery after treatment intervention in basal ganglia disorders.

Indexed as

AnimalsCorpus StriatumDisease Models, AnimalHumansHuntington DiseaseMiceMice, TransgenicNeuronsCalcium imagingHuntington’s diseaseNetworkNeuronal activityStriatum

Identifiers

PMID32466798
PMCPMC7254676
OpenAlexW3032063460

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.