Evidence map›Paper›PMID 36360174›Full record

ReviewGenes2022

Human Induced Pluripotent Stem Cell Phenotyping and Preclinical Modeling of Familial Parkinson's Disease.

Jeffrey Kim, Etienne W Daadi, Thomas Oh, Elyas S Daadi, Marcel M Daadi

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Cells · 2023
    Article
  8. Review
  9. 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

5 authors at 2 institutions in 1 country.

Jeffrey KimSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
Etienne W DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
Thomas OhSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
Elyas S DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
Marcel M DaadiSouthwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, TX 78227, USA.
Texas Biomedical Research Institute · USThe University of Texas 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 OD011133NIH HHS R56 AG059284
6 · The paper itself

Abstract

Parkinson's disease (PD) is primarily idiopathic and a highly heterogenous neurodegenerative disease with patients experiencing a wide array of motor and non-motor symptoms. A major challenge for understanding susceptibility to PD is to determine the genetic and environmental factors that influence the mechanisms underlying the variations in disease-associated traits. The pathological hallmark of PD is the degeneration of dopaminergic neurons in the substantia nigra pars compacta region of the brain and post-mortem Lewy pathology, which leads to the loss of projecting axons innervating the striatum and to impaired motor and cognitive functions. While the cause of PD is still largely unknown, genome-wide association studies provide evidence that numerous polymorphic variants in various genes contribute to sporadic PD, and 10 to 15% of all cases are linked to some form of hereditary mutations, either autosomal dominant or recessive. Among the most common mutations observed in PD patients are in the genes LRRK2, SNCA, GBA1, PINK1, PRKN, and PARK7/DJ-1. In this review, we cover these PD-related mutations, the use of induced pluripotent stem cells as a disease in a dish model, and genetic animal models to better understand the diversity in the pathogenesis and long-term outcomes seen in PD patients.

Indexed as

Induced Pluripotent Stem CellsNeurodegenerative DiseasesParkinson DiseaseAnimalsDopaminergic NeuronsGenome-Wide Association StudyHumansbrain organoidsgenetic basis for pathophysiologyinduced pluripotent stem cellsin vitro models of familial Parkinson’s diseaseParkinson’s diseasepersonalized medicine

Identifiers

PMID36360174
PMCPMC9689743
OpenAlexW4307237977

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.