Evidence map›Paper›PMID 29422836›Full record

ArticleFrontiers in neuroscience2018

Early Alterations in Operant Performance and Prominent Huntingtin Aggregation in a Congenic F344 Rat Line of the Classical CAG

Anne-Christine Plank, Fabio Canneva, Kerstin A Raber, Yvonne K Urbach, Julia Dobner, Maja Puchades, Jan G Bjaalie, Clarissa Gillmann, Tobias Bäuerle, Olaf Riess and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

12 authors at 2 institutions in 2 countries.

Anne-Christine PlankExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
Fabio CannevaExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
Kerstin A RaberExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
Yvonne K UrbachExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
Julia DobnerExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
Maja PuchadesNeural Systems Laboratory, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Jan G BjaalieNeural Systems Laboratory, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Clarissa GillmannPreclinical Imaging Platform Erlangen, Institute of Radiology, University Clinics Erlangen, Erlangen, Germany.
Tobias BäuerlePreclinical Imaging Platform Erlangen, Institute of Radiology, University Clinics Erlangen, Erlangen, Germany.
Olaf RiessInstitute of Medical Genetics and Applied Genomics, University Clinics Tuebingen, Tuebingen, Germany.
Hoa H P NguyenInstitute of Medical Genetics and Applied Genomics, University Clinics Tuebingen, Tuebingen, Germany.
Stephan von HörstenExperimental Therapy, Preclinical Experimental Center, University Clinics Erlangen, Erlangen, Germany.
University of Oslo · NOUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transgenic rat model of Huntington disease expressing a fragment of mutant HTT (tgHD rat) has been thoroughly characterized and reproduces hallmark symptoms of human adult-onset HD. Pursuing the optimization of this model for evaluation of translational therapeutic approaches, the F344 inbred rat strain was considered as advantageous genetic background for the expression of the HD transgenic construct. In the present study, a novel congenic line of the SPRDtgHD transgenic model of HD, carrying 51 CAG repeats, was generated on the F344 rat genetic background. To assess the behavioral phenotype, classical assays investigating motor function, emotion, and sensorimotor gating were applied, along with automated screening of metabolic and activity parameters as well as operant conditioning tasks. The neuropathological phenotype was analyzed by immunohistochemistry and

Indexed as

behavioral phenotypingF344 rathuntingtin aggregatesHuntington diseaseoperant conditioningtransgenic rat model

Identifiers

PMID29422836
PMCPMC5788972
OpenAlexW2792915296

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.