Evidence map›Paper›PMID 31520365›Full record

ArticleJournal of molecular neuroscience : MN2020

Deletion of the Creatine Transporter (Slc6a8) in Dopaminergic Neurons Leads to Hyperactivity in Mice.

Zuhair I Abdulla, Bahar Pahlevani, Kerstin H Lundgren, Jordan L Pennington, Kenea C Udobi, Kim B Seroogy, Matthew R Skelton

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. [Scientific reports · 2025
    Article
  3. Article
  4. Article
  5. Attention-deficit/hyperactive disorder updates.Frontiers in molecular neuroscience · 2022
    Review
  6. Review
  7. Article
  8. Review
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 4 institutions in 2 countries.

Zuhair I AbdullaDepartment of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation, Cincinnati, OH, USA.
Bahar PahlevaniDepartment of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation, Cincinnati, OH, USA.
Kerstin H LundgrenDepartment of Neurology, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.
Jordan L PenningtonDepartment of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation, Cincinnati, OH, USA.
Kenea C UdobiDepartment of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation, Cincinnati, OH, USA.
Kim B SeroogyDepartment of Neurology, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.
Matthew R SkeltonDepartment of Pediatrics, University of Cincinnati College of Medicine and Division of Neurology, Cincinnati Children's Research Foundation, Cincinnati, OH, USA. Matthew.skelton@cchmc.org.ORCID http://orcid.org/0000-0003-4941-3546
Cincinnati Children's Hospital Medical Center · USHospital Research Foundation · AUUniversity of Cincinnati · USUniversity of Cincinnati Medical Center · US

Funding

The role of Na+, K+-ATPase function in Creatine Transporter DeficiencyR21HD080910 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI SKELTON, MATTHEW R · 2015 to 2016
$441k
NICHD NIH HHS R21 HD080910NIH HHS HD080910
6 · The paper itself

Abstract

The lack of cerebral creatine (Cr) causes intellectual disability and epilepsy. In addition, a significant portion of individuals with Cr transporter (Crt) deficiency (CTD), the leading cause of cerebral Cr deficiency syndromes (CCDS), are diagnosed with attention-deficit hyperactivity disorder. While the neurological effects of CTD are clear, the mechanisms that underlie these deficits are unknown. Part of this is due to the heterogenous nature of the brain and the unique metabolic demands of specific neuronal systems. Of particular interest related to Cr physiology are dopaminergic neurons, as many CCDS patients have ADHD and Cr has been implicated in dopamine-associated neurodegenerative disorders, such as Parkinson's and Huntington's diseases. The purpose of this study was to examine the effect of a loss of the Slc6a8 (Crt) gene in dopamine transporter (Slc6a3; DAT) expressing cells on locomotor activity and motor function as the mice age. Floxed Slc6a8 (Slc6a8

Indexed as

LocomotionAnimalsBrain Diseases, Metabolic, InbornCreatineDopaminergic NeuronsGene DeletionMaleMembrane Transport ProteinsMiceMice, Inbred C57BLPlasma Membrane Neurotransmitter Transport ProteinsX-Linked Intellectual DisabilityCreatinecreatine transporterMembrane Transport ProteinsPlasma Membrane Neurotransmitter Transport ProteinsCreatineCreatine transporterDAT-CreHyperactivityMotor function

Identifiers

PMID31520365
PMCPMC7001766
OpenAlexW2972334560

What OpenQuestion holds

Textmetadata
LicenceTDM
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.