Evidence map›Paper›PMID 30626701›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Loss-of-Huntingtin in Medial and Lateral Ganglionic Lineages Differentially Disrupts Regional Interneuron and Projection Neuron Subtypes and Promotes Huntington's Disease-Associated Behavioral, Cellular, and Pathological Hallmarks.

Mark F Mehler, Jenna R Petronglo, Eduardo E Arteaga-Bracho, Maria E Gulinello, Michael L Winchester, Nandini Pichamoorthy, Stephen K Young, Christopher D DeJesus, Hifza Ishtiaq, Solen Gokhan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  17. Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
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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

11 authors at 3 institutions in 6 countries.

Mark F MehlerRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Jenna R PetrongloRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.ORCID 0000-0001-9969-6607
Eduardo E Arteaga-BrachoRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Maria E GulinelloDominick P. Purpura Department of Neuroscience.ORCID 0000-0002-4647-9622
Michael L WinchesterRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Nandini PichamoorthyRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Stephen K YoungRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Christopher D DeJesusRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Hifza IshtiaqRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Solen GokhanRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine.
Aldrin E MoleroRoslyn and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine, aldrin.molero@einstein.yu.edu.ORCID 0000-0001-8250-1236
John F. Kennedy Center for the Performing Arts · USAlbert Einstein College of Medicine · USInstitute for Stem Cell Biology and Regenerative Medicine · IN

Funding

Support for the Rose F. Kennedy IDDRCU54HD090260 · NICHD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WALKLEY, STEVEN UPSHAW · 2016 to 2020
$6.0M
Translational Neuroimaging CoreP30HD071593 · NICHD · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WALKLEY, STEVEN UPSHAW · 2011 to 2015
$5.6M
Huntington's disease: a novel developmental oligodendrogliopathyR01NS096144 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MEHLER, MARK F · 2016 to 2020
$1.8M
The Role of Huntingtin in Striatal NeurogenesisR01NS073758 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MOLERO, ALDRIN ENRIQUE · 2011 to 2015
$1.6M
Neurodegenerative Diseases: A New Class of Primary Developmental Disorders?R01NS071571 · NINDS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI MEHLER, MARK F · 2010 to 2013
$1.3M
NICHD NIH HHS P30 HD071593NICHD NIH HHS U54 HD090260NINDS NIH HHS R01 NS071571NINDS NIH HHS R01 NS073758NINDS NIH HHS R01 NS096144
6 · The paper itself

Abstract

Emerging studies are providing compelling evidence that the pathogenesis of Huntington's disease (HD), a neurodegenerative disorder with frequent midlife onset, encompasses developmental components. Moreover, our previous studies using a hypomorphic model targeting huntingtin during the neurodevelopmental period indicated that loss-of-function mechanisms account for this pathogenic developmental component (Arteaga-Bracho et al., 2016). In the present study, we specifically ascertained the roles of subpallial lineage species in eliciting the previously observed HD-like phenotypes. Accordingly, we used the Cre-loxP system to conditionally ablate the murine huntingtin gene (Htt

Indexed as

AnimalsAnxietyBehavior, AnimalBrainCorpus StriatumFemaleGlobus PallidusHuntingtin ProteinHuntington DiseaseInterneuronsMaleMice, Inbred C57BLMice, KnockoutMotor CortexNeuronsProsencephalonHtt protein, mouseHuntingtin ProteinReelin ProteinRELN protein, humanReln protein, mousecell vulnerabilitydevelopmentinterneuronsneurodegenerationpathogenesissubpallium

Identifiers

PMID30626701
PMCPMC6407290
OpenAlexW2910489549

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.