Evidence map›Paper›PMID 38608784›Full record

ArticleNeurobiology of disease2024

BDNF and TRiC-inspired reagent rescue cortical synaptic deficits in a mouse model of Huntington's disease.

Yingli Gu, Alexander Pope, Charlene Smith, Christopher Carmona, Aaron Johnstone, Linda Shi, Xuqiao Chen, Sarai Santos, Claire Cecile Bacon-Brenes, Thomas Shoff and 5 more

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2024. 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
1.9field-weighted citation impact, top 16% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  2. Review
  3. Disruption of BDNF signalling in neuropathologies.Biochemical Society transactions · 2026
    Review
  4. 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

15 authors at 5 institutions in 2 countries.

Yingli GuDepartment of Neurology, The Fourth Hospital of Harbin Medical University, 150001, China; Department of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Alexander PopeDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Charlene SmithDepartment of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States of America.
Christopher CarmonaDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America; Department of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States of America; Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, United States of America; Beckman Laser Institute & Medical Clinic, University of California, Irvine, Irvine, CA, United States; Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, United States.
Aaron JohnstoneDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Linda ShiDepartment of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States of America; Department of Bioengineering, University of California San Diego, La Jolla, CA 92093, United States of America; Beckman Laser Institute & Medical Clinic, University of California, Irvine, Irvine, CA, United States; Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, United States.
Xuqiao ChenDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Sarai SantosDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Claire Cecile Bacon-BrenesNeuroscience, Scripps College, Claremont, CA 91711, United States of America.
Thomas ShoffDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America.
Korbin M KleczkoDepartment of Biology and Genetics, Stanford University, Stanford, CA 94305-5430, United States of America.
Judith FrydmanDepartment of Biology and Genetics, Stanford University, Stanford, CA 94305-5430, United States of America.
Leslie M ThompsonDepartment of Psychiatry and Human Behavior, University of California, Irvine, CA 92697, United States of America; Institute of Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697, United States of America; Department of Neurobiology and Behavior, University of California, Irvine, CA 92697, United States of America; Sue and Bill Gross Stem Cell Center, University of California, Irvine, CA 92697, United States of America.
William C MobleyDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America. Electronic address: wmobley@health.ucsd.edu.
Chengbiao WuDepartment of Neurosciences, University of California San Diego, La Jolla, CA 92093, United States of America. Electronic address: chw049@health.ucsd.edu.
University of California, San Diego · USUniversity of California, Irvine · USStanford University · USFourth Affiliated Hospital of Harbin Medical University · CNScripps College · US

Funding

Molecular Mechanisms of Pathogenesis in Huntington’s diseaseR35NS116872 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Leslie Michels Thompson · 2020 to 2026
$8.5M
Mechanism of the Eukaryotic Chaperonin TRiC/CCTR01GM074074 · NIGMS · STANFORD UNIVERSITY · PI FRYDMAN, JUDITH · 2005 to 2024
$6.8M
Project 3: TRiC modulation of CNS pathogenesis in HD mouse modelsP01NS092525 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI THOMPSON, LESLIE MICHELS · 2016 to 2020
$6.3M
NIGMS NIH HHS R01 GM074074NINDS NIH HHS P01 NS092525NINDS NIH HHS R35 NS116872
6 · The paper itself

Abstract

Synaptic changes are early manifestations of neuronal dysfunction in Huntington's disease (HD). However, the mechanisms by which mutant HTT protein impacts synaptogenesis and function are not well understood. Herein we explored HD pathogenesis in the BACHD mouse model by examining synaptogenesis and function in long term primary cortical cultures. At DIV14 (days in vitro), BACHD cortical neurons showed no difference from WT neurons in synaptogenesis as revealed by colocalization of a pre-synaptic (Synapsin I) and a post-synaptic (PSD95) marker. From DIV21 to DIV35, BACHD neurons showed progressively reduced colocalization of Synapsin I and PSD95 relative to WT neurons. The deficits were effectively rescued by treatment of BACHD neurons with BDNF. The recombinant apical domain of CCT1 (ApiCCT1) yielded a partial rescuing effect. BACHD neurons also showed culture age-related significant functional deficits as revealed by multielectrode arrays (MEAs). These deficits were prevented by BDNF, whereas ApiCCT1 showed a less potent effect. These findings are evidence that deficits in BACHD synapse and function can be replicated in vitro and that BDNF or a TRiC-inspired reagent can potentially be protective against these changes in BACHD neurons. Our findings support the use of cellular models to further explicate HD pathogenesis and potential treatments.

Indexed as

Brain-Derived Neurotrophic FactorCerebral CortexDisease Models, AnimalHuntington DiseaseNeuronsSynapsesAnimalsCells, CulturedHuntingtin ProteinMiceMice, Inbred C57BLMice, TransgenicSynapsinsBdnf protein, mouseBrain-Derived Neurotrophic FactorHuntingtin ProteinSynapsinsBACHDBrain-derived neurotrophic factorCortical neuronsHuntington's diseaseLong term cultureMulti-array electrodeNeuronal activityPre- and post-synapticPSD95SynapseTRiC

Identifiers

PMID38608784
PMCPMC11890210
OpenAlexW4394694039

What Socratic 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 Socratic graph.