Evidence map›Paper›PMID 29550604›Full record

ReviewNeurochemistry international2018

Current perspective of mitochondrial biology in Parkinson's disease.

Navneet Ammal Kaidery, Bobby Thomas

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurochemistry international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
8.8field-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

51 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. GALNT9 enrichment attenuates MPPBiology direct · 2024
    Article
  7. Review
  8. Research progress on intranasal treatment for Parkinson's disease.Neuroprotection (Chichester, England) · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Consequences of Disturbing Manganese Homeostasis.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Review
  15. A Brief Review of Low-Level Light Therapy in Depression Disorder.Journal of lasers in medical sciences · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Navneet Ammal KaideryDepartments of Pharmacology and Toxicology, Augusta, GA 30912, United States.
Bobby ThomasDepartments of Pharmacology and Toxicology, Augusta, GA 30912, United States; Neurology Medical College of Georgia, Augusta University, Augusta, GA 30912, United States. Electronic address: bthomas1@augusta.edu.
Augusta University · US

Funding

Role of Bach-1-Mediated Transcriptional Regulation in NeuroprotectionR01NS101967 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI THOMAS, BOBBY · 2017 to 2021
$1.9M
NINDS NIH HHS R01 NS101967
6 · The paper itself

Abstract

Parkinson's disease (PD) is one of the most common neurodegenerative movement disorder characterized by preferential loss of dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies containing α-synuclein. Although the cause of PD remains elusive, remarkable advances have been made in understanding the possible causative mechanisms of PD pathogenesis. An explosion of discoveries during the past two decades has led to the identification of several autosomal dominant and recessive genes that cause familial forms of PD. The investigations of these familial PD gene products have shed considerable insights into the molecular pathogenesis of the more common sporadic PD. A growing body of evidence suggests that the etiology of PD is multifactorial and involves a complex interplay between genetic and environmental factors. Substantial evidence from human tissues, genetic and toxin-induced animal and cellular models indicates that mitochondrial dysfunction plays a central role in the pathophysiology of PD. Deficits in mitochondrial functions due to bioenergetics defects, alterations in the mitochondrial DNA, generation of reactive oxygen species, aberrant calcium homeostasis, and anomalies in mitochondrial dynamics and quality control are implicated in the underlying mechanisms of neuronal cell death in PD. In this review, we discuss how familial PD-linked genes and environmental factors interface the pathways regulating mitochondrial functions and thereby potentially converge both familial and sporadic PD at the level of mitochondrial integrity. We also provide an overview of the status of therapeutic strategies targeting mitochondrial dysfunction in PD. Unraveling potential pathways that influence mitochondrial homeostasis in PD may hold the key to therapeutic intervention for this debilitating neurodegenerative movement disorder.

Indexed as

AnimalsDopaminergic NeuronsHumansMitochondriaMitochondrial DynamicsOxidative StressParkinson DiseaseMitochondrial DNAMitochondrial dynamicsOxidative phosphorylationParkinson's diseasePermeability transition poreReactive oxygen species

Identifiers

PMID29550604
PMCPMC6027640
OpenAlexW2792072456

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.