Evidence map›Paper›PMID 28057534›Full record

ArticleNeuroscience2017

Altered fronto-striatal functions in the Gdi1-null mouse model of X-linked Intellectual Disability.

Lorenzo Morè, Basil Künnecke, Latefa Yekhlef, Andreas Bruns, Antonella Marte, Ernesto Fedele, Veronica Bianchi, Stefano Taverna, Silvia Gatti, Patrizia D'Adamo

Abstract read
In one paragraph

Article in Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Aging · 2021
    Article
  4. 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

10 authors.

Lorenzo MorèMolecular Genetics of Intellectual Disability Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Basil KünneckepRED, Pharma Research & Early Development, NORD Neuroscience, Roche Innovation Center Basel, F. Hoffmann-La Roche AG, Switzerland.
Latefa YekhlefNeuroimmunology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Andreas BrunspRED, Pharma Research & Early Development, NORD Neuroscience, Roche Innovation Center Basel, F. Hoffmann-La Roche AG, Switzerland.
Antonella MarteDepartment of Pharmacy, Section of Pharmacology and Toxicology, Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy.
Ernesto FedeleDepartment of Pharmacy, Section of Pharmacology and Toxicology, Center of Excellence for Biomedical Research, University of Genoa, Genoa, Italy.
Veronica BianchiMolecular Genetics of Intellectual Disability Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Stefano TavernaNeuroimmunology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Silvia GattipRED, Pharma Research & Early Development, NORD Neuroscience, Roche Innovation Center Basel, F. Hoffmann-La Roche AG, Switzerland.
Patrizia D'AdamoMolecular Genetics of Intellectual Disability Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. Electronic address: dadamo.patrizia@hsr.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RAB-GDP dissociation inhibitor 1 (GDI1) loss-of-function mutations are responsible for a form of non-specific X-linked Intellectual Disability (XLID) where the only clinical feature is cognitive impairment. GDI1 patients are impaired in specific aspects of executive functions and conditioned response, which are controlled by fronto-striatal circuitries. Previous molecular and behavioral characterization of the Gdi1-null mouse revealed alterations in the total number/distribution of hippocampal and cortical synaptic vesicles as well as hippocampal short-term synaptic plasticity, and memory deficits. In this study, we employed cognitive protocols with high translational validity to human condition that target the functionality of cortico-striatal circuitry such as attention and stimulus selection ability with progressive degree of complexity. We previously showed that Gdi1-null mice are impaired in some hippocampus-dependent forms of associative learning assessed by aversive procedures. Here, using appetitive-conditioning procedures we further investigated associative learning deficits sustained by the fronto-striatal system. We report that Gdi1-null mice are impaired in attention and associative learning processes, which are a key part of the cognitive impairment observed in XLID patients.

Indexed as

AmygdalaAnimalsAssociation LearningAttentionConditioning, PsychologicalDiscrimination, PsychologicalDisease Models, AnimalDopamineExcitatory Postsynaptic PotentialsFrontal LobeGuanine Nucleotide Dissociation InhibitorsInhibition, PsychologicalIntellectual DisabilityMaleMice, KnockoutNeostriatumDopamineGDP dissociation inhibitor 1Guanine Nucleotide Dissociation Inhibitorsappetitive conditioningexcitatory synapsesfronto-striatal synaptic plasticityGdi1-null miceX-linked Intellectual Disability

Identifiers

PMID28057534
PMCPMC5315088

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.