Evidence map›Paper›PMID 26225560›Full record

ArticlePloS one2015

Therapeutic Effect of Berberine on Huntington's Disease Transgenic Mouse Model.

Wenxiao Jiang, Wenjie Wei, Marta A Gaertig, Shihua Li, Xiao-Jiang Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
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  12. Research progress on pharmacological effects and bioavailability of berberine.Naunyn-Schmiedeberg's archives of pharmacology · 2024
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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

5 authors at 2 institutions in 2 countries.

Wenxiao JiangDepartment of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, United States of America; Graduate Program of Microbiology and Molecular Genetics, Emory University, Atlanta, GA 30322, United States of America.
Wenjie WeiDepartment of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, United States of America; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430032, China.
Marta A GaertigDepartment of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, United States of America.
Shihua LiDepartment of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, United States of America.
Xiao-Jiang LiDepartment of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, GA 30322, United States of America.
Emory University · USTongji Hospital · CN

Funding

Neuronal function of huntingtin-associated proteinR01NS036232 · NINDS · EMORY UNIVERSITY · PI ESCAYG, ANDREW P · 1998 to 2021
$6.7M
Nuclear Toxicity of Huntington Disease ProteinR01NS041669 · NINDS · EMORY UNIVERSITY · PI LI, XIAO-JIANG · 2001 to 2015
$4.6M
Synaptic toxicity of Huntington disease proteinR01AG019206 · NIA · EMORY UNIVERSITY · PI LI, XIAO-JIANG · 2001 to 2016
$4.5M
Polyglutamine expansion and neuropathologyR01NS045016 · NINDS · EMORY UNIVERSITY · PI LI, SHI-HUA · 2004 to 2013
$2.9M
Glial huntingtin and neuronal excitotoxicityR01AG031153 · NIA · EMORY UNIVERSITY · PI LI, SHI-HUA · 2009 to 2013
$1.5M
Synaptic accumulation of misfolded proteins and neurodegenerationR56AG019206 · NIA · EMORY UNIVERSITY · PI JIN, PENG · 2018 to 2018
$489k
NIA NIH HHS AG019206NIA NIH HHS R01 AG019206NIA NIH HHS R01 AG031153NIA NIH HHS R56 AG019206NINDS NIH HHS NS036232NINDS NIH HHS NS041669NINDS NIH HHS R01 NS036232NINDS NIH HHS R01 NS041669NINDS NIH HHS R01 NS045016
6 · The paper itself

Abstract

Huntington disease (HD) represents a family of neurodegenerative diseases that are caused by misfolded proteins. The misfolded proteins accumulate in the affected brain regions in an age-dependent manner to cause late-onset neurodegeneration. Transgenic mouse models expressing the HD protein, huntingtin, have been widely used to identify therapeutics that may retard disease progression. Here we report that Berberine (BBR), an organic small molecule isolated from plants, has protective effects on transgenic HD (N171-82Q) mice. We found that BBR can reduce the accumulation of mutant huntingtin in cultured cells. More importantly, when given orally, BBR could effectively alleviate motor dysfunction and prolong the survival of transgenic N171-82Q HD mice. We found that BBR could promote the degradation of mutant huntingtin by enhancing autophagic function. Since BBR is an orally-taken drug that has been safely used to treat a number of diseases, our findings suggest that BBR can be tested on different HD animal models and HD patients to further evaluate its therapeutic effects.

Indexed as

Disease Models, AnimalAnimalsAutophagyBehavior, AnimalBerberineHEK293 CellsHumansHuntington DiseaseMiceMice, TransgenicBerberine

Identifiers

PMID26225560
PMCPMC4520448
OpenAlexW1896472383

What OpenQuestion 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 OpenQuestion graph.