Evidence map›Paper›PMID 34762921›Full record

ArticleExperimental neurology2022

Dopamine D3 receptor ligand suppresses the expression of levodopa-induced dyskinesia in nonhuman primate model of parkinson's disease.

Thomas Oh, Elyas S Daadi, Jeffrey Kim, Etienne W Daadi, Peng-Jen Chen, Gourav Roy-Choudhury, Jonathan Bohmann, Benjamin E Blass, Marcel M Daadi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

9 authors at 4 institutions in 1 country.

Thomas OhSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA.
Elyas S DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA.
Jeffrey KimSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA; Cell Systems & Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA.
Etienne W DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA.
Peng-Jen ChenDepartment of Pharmaceutical Sciences, Moulder Center for Drug Discovery Research, Temple University School of Pharmacy, Philadelphia, PA, USA.
Gourav Roy-ChoudhurySouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA.
Jonathan BohmannSouthwest Research Institute, San Antonio, TX, USA.
Benjamin E BlassDepartment of Pharmaceutical Sciences, Moulder Center for Drug Discovery Research, Temple University School of Pharmacy, Philadelphia, PA, USA.
Marcel M DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX, USA; Cell Systems & Anatomy, University of Texas Health at San Antonio, San Antonio, TX, USA; Radiology, Long School of Medicine, University of Texas Health at San Antonio, San Antonio, TX, USA. Electronic address: mdaadi@txbiomed.org.
Texas Biomedical Research Institute · USTemple University · USSouthwest Research Institute · USThe University of Texas Health Science Center at San Antonio · US

Funding

The Southwest National Primate Research Center Supplement- Infrastructure improvements of ABSL2 holding areasP51OD011133 · OD · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI Larry S. Schlesinger · 2012 to 2026
$129.7M
Impact of Physical Activity on Striatal Reinnervation in a Nonhuman Primate Model of Parkinson's DiseaseR56AG059284 · NIA · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI DAADI, MARCEL · 2018 to 2018
$710k
NIA NIH HHS R56 AG059284NIH HHS P51 OD011133
6 · The paper itself

Abstract

Parkinson's disease (PD) is a complex multisystem, chronic and so far incurable disease with significant unmet medical needs. The incidence of PD increases with aging and the expected burden will continue to escalate with our aging population. Since its discovery in the 1961 levodopa has remained the gold standard pharmacotherapy for PD. However, the progressive nature of the neurodegenerative process in and beyond the nigrostriatal system causes a multitude of side effects, including levodopa-induced dyskinesia within 5 years of therapy. Attenuating dyskinesia has been a significant challenge in the clinical management of PD. We report on a small molecule that eliminates the expression of levodopa-induced dyskinesia and significantly improves PD-like symptoms. The lead compound PD13R we discovered is a dopamine D3 receptor partial agonist with high affinity and selectivity, orally active and with desirable drug-like properties. Future studies are aimed at developing this lead compound for treating PD patients with dyskinesia.

Indexed as

AnimalsAntiparkinson AgentsCallithrixDopamine AgentsDopamine AgonistsDyskinesia, Drug-InducedHEK293 CellsHumansLevodopaLigandsParkinsonian DisordersPrimatesProtein Structure, SecondaryQuinpiroleReceptors, Dopamine D3Antiparkinson AgentsDopamine AgentsDopamine AgonistsLevodopaLigandsQuinpiroleReceptors, Dopamine D3ActigraphyArylpiperazine pharmacophoreD3 receptorLevodopa-induced dyskinesiaNonhuman primate model of dyskinesiaParkinson's diseaseSleep disturbances

Identifiers

PMID34762921
PMCPMC13102547
OpenAlexW3214149663

What OpenQuestion holds

Textmetadata
LicenceTDM
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.