Evidence map›Paper›PMID 41720207›Full record

ArticleExperimental neurology2026

Glucose transporter 3 gene deficiency modifies Huntington's disease progression in zQ175 model mice.

Tomoko Daida, Bo-Chul Shin, Joshua Barry, Theresa Da Silva, Deneen Argueta, Lauren Cheng, Yasemin Ozay, Carlos Cepeda, Sherin U Devaskar

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Tomoko DaidaDepartment of Pediatrics, Division of Neonatology and Developmental Biology and Neonatal Research Center at UCLA, Children's Discovery and Innovation Institute at UCLA, Los Angeles, CA, USA.
Bo-Chul ShinDepartment of Pediatrics, Division of Neonatology and Developmental Biology and Neonatal Research Center at UCLA, Children's Discovery and Innovation Institute at UCLA, Los Angeles, CA, USA.
Joshua BarryIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Theresa Da SilvaIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Deneen ArguetaIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Lauren ChengIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Yasemin OzayDepartment of Pediatrics, Division of Neonatology and Developmental Biology and Neonatal Research Center at UCLA, Children's Discovery and Innovation Institute at UCLA, Los Angeles, CA, USA.
Carlos CepedaIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Sherin U DevaskarDepartment of Pediatrics, Division of Neonatology and Developmental Biology and Neonatal Research Center at UCLA, Children's Discovery and Innovation Institute at UCLA, Los Angeles, CA, USA. Electronic address: sdevaskar@mednet.ucla.edu.

Funding

Prenatal Origins of Neurometabolic ConsequencesR01HD081206 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2015 to 2024
$4.1M
Deficient Neuronal Glucose Transport Underlies Cortical Hyperexcitability in Mouse Models of Huntington’s DiseaseR21NS123883 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CEPEDA, CARLOS T, DEVASKAR, SHERIN U · 2022 to 2023
$429k
NICHD NIH HHS R01 HD081206NINDS NIH HHS R21 NS123883
6 · The paper itself

Abstract

In Huntington's disease (HD), reduced neuronal glucose transport plays an important role. We investigated the effects of GLUT3 knock-down (KD) on the trajectory of the HD phenotype in zQ175 model mice. GLUT3 (G3) expression was reduced in heterozygous (HT) and homozygous mice. zQ175 mice when crossed with Emx1-G3KD HT mice, created conditional GLUT3-KD in cortical pyramidal neurons (CPNs), allowing examination of Q175WT/G3WT, Q175WT/G3KD, Q175HT/G3WT, and Q175HT/G3KD genotypes. Immunohistochemically, higher GLUT3 expression and number of GLUT3 positive CPNs were observed in Q175WT/G3WT compared to Q175WT/G3KD, Q175HT/G3WT, and Q175HT/G3KD, with no difference among these three groups, supporting a protective floor effect. Behaviorally, Q175HT/G3KD mice faced difficulty learning tasks and thereby performed worse than the other three groups. Electrophysiologically, the basic membrane properties of cortical pyramidal neurons (CPNs) were not affected. In contrast, in striatal medium-sized spiny neurons (MSNs) significant increases in cell membrane input resistance occurred in Q175HT/G3WT and Q175HT/G3KD compared to Q175WT/G3WT and Q175WT/G3KD, with no difference between Q175HT/G3WT and Q175HT/G3KD. Upon examination of spontaneous glutamatergic and GABAergic synaptic currents, the cumulative interevent intervals (IEI) revealed increased glutamatergic activity in GLUT3 KD, suggesting increased cortical excitability, with a concomitant compensatory increase in GABA synaptic activity. In striatal MSNs, a subtle but significant decrease in sEPSCs frequency occurred between Q175HT/G3WT and Q175HT/G3KD. The key change was an increase in frequency of sIPSCs in Q175HT/G3WT and Q175HT/G3KD compared to Q175WT/G3WT. These results underscore complex modifications of the HD phenotype among groups related to the interplay between GLUT3 KD, compensatory mechanisms, and floor effects.

Indexed as

Glucose Transporter Type 3Huntington DiseaseAnimalsDisease Models, AnimalDisease ProgressionMaleMiceMice, TransgenicPyramidal CellsGlucose Transporter Type 3ElectrophysiologyGlucose transporter 3 (GLUT3)Huntington's diseaseKnock-downMurine models

Identifiers

PMID41720207
PMCPMC13326910

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.