Evidence map›Paper›PMID 38627765›Full record

ArticleJournal of biomedical science2024

Attenuating mitochondrial dysfunction and morphological disruption with PT320 delays dopamine degeneration in MitoPark mice.

Vicki Wang, Kuan-Yin Tseng, Tung-Tai Kuo, Eagle Yi-Kung Huang, Kuo-Lun Lan, Zi-Rong Chen, Kuo-Hsing Ma, Nigel H Greig, Jin Jung, Ho-Ii Choi and 3 more

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In one paragraph

Article in Journal of biomedical science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 2% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

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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

13 authors at 6 institutions in 3 countries.

Vicki WangDoctoral Degree Program in Translational Medicine, National Defense Medical Center and Academia Sinica, Taipei, 11490, Taiwan.
Kuan-Yin TsengDepartment of Neurological Surgery, Tri-Service General Hospital, Taipei, 11490, Taiwan.
Tung-Tai KuoDepartment of Neurological Surgery, Tri-Service General Hospital, Taipei, 11490, Taiwan.
Eagle Yi-Kung HuangDepartment of Pharmacology, National Defense Medical Center, Taipei, 11490, Taiwan.
Kuo-Lun LanDepartment of Pathology, Tri-Service General Hospital, Taipei, 11490, Taiwan.
Zi-Rong ChenDepartment of Pathology, Tri-Service General Hospital, Taipei, 11490, Taiwan.
Kuo-Hsing MaGraduate Institute of Biology and Anatomy, National Defense Medical Center, Taipei, 11490, Taiwan.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD, 21224, USA.
Jin JungPeptron, Inc., Yuseong-gu, Daejeon, 34054, Republic of Korea.
Ho-Ii ChoiPeptron, Inc., Yuseong-gu, Daejeon, 34054, Republic of Korea.
Lars OlsonDepartment of Neuroscience, Karolinska Institute, 171 77, Stockholm, Sweden.
Barry J HofferDepartment of Neurosurgery, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Yuan-Hao ChenDepartment of Neurological Surgery, Tri-Service General Hospital, Taipei, 11490, Taiwan. chenyh178@gmail.com.ORCID http://orcid.org/0000-0002-0570-4328
Tri-Service General Hospital · TWNational Defense Medical Center · TWFlex (United States) · USKarolinska Institutet · SENational Institutes of Health · USUniversity Hospitals of Cleveland · US

Funding

Neuroprotective role of GLP-1 receptor agonists (Neurodegenerative disorders & Alzheimer's disease)ZIAAG000333 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$10.9M
NIA NIH HHS AG000333
6 · The paper itself

Abstract

backgroundMitochondria are essential organelles involved in cellular energy production. Changes in mitochondrial function can lead to dysfunction and cell death in aging and age-related disorders. Recent research suggests that mitochondrial dysfunction is closely linked to neurodegenerative diseases. Glucagon-like peptide-1 receptor (GLP-1R) agonist has gained interest as a potential treatment for Parkinson's disease (PD). However, the exact mechanisms responsible for the therapeutic effects of GLP-1R-related agonists are not yet fully understood.

methodsIn this study, we explores the effects of early treatment with PT320, a sustained release formulation of the GLP-1R agonist Exenatide, on mitochondrial functions and morphology in a progressive PD mouse model, the MitoPark (MP) mouse.

resultsOur findings demonstrate that administration of a clinically translatable dose of PT320 ameliorates the reduction in tyrosine hydroxylase expression, lowers reactive oxygen species (ROS) levels, and inhibits mitochondrial cytochrome c release during nigrostriatal dopaminergic denervation in MP mice. PT320 treatment significantly preserved mitochondrial function and morphology but did not influence the reduction in mitochondria numbers during PD progression in MP mice. Genetic analysis indicated that the cytoprotective effect of PT320 is attributed to a reduction in the expression of mitochondrial fission protein 1 (Fis1) and an increase in the expression of optic atrophy type 1 (Opa1), which is known to play a role in maintaining mitochondrial homeostasis and decreasing cytochrome c release through remodeling of the cristae.

conclusionOur findings suggest that the early administration of PT320 shows potential as a neuroprotective treatment for PD, as it can preserve mitochondrial function. Through enhancing mitochondrial health by regulating Opa1 and Fis1, PT320 presents a new neuroprotective therapy in PD.

Indexed as

Cytochromes cExenatideGlucagon-Like Peptide-1 Receptor AgonistsMitochondrial DiseasesDisease Models, AnimalParkinson DiseaseCytochromes cExenatideGlucagon-Like Peptide-1 Receptor AgonistsExenatideGlucagon-like peptide-1 receptor agonistMitochondriaMitoPark mouseParkinson’s diseasePT320

Identifiers

PMID38627765
PMCPMC11022395
OpenAlexW4394869555

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.