Evidence map›Paper›PMID 29700661›Full record

ReviewCellular and molecular neurobiology2018

Parkinson Disease from Mendelian Forms to Genetic Susceptibility: New Molecular Insights into the Neurodegeneration Process.

Amin Karimi-Moghadam, Saeid Charsouei, Benjamin Bell, Mohammad Reza Jabalameli

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Genetic mutations in Parkinson's disease: screening of a selected population from North-Eastern Italy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  15. Article
  16. GBA-associated Parkinson's disease in Hungary: clinical features and genetic insights.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  17. Review
  18. Article
  19. Involvement of Mitochondria in Parkinson's Disease.International journal of molecular sciences · 2023
    Review
  20. Article

10 more citing papers are in PubMed but not listed here.

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

4 authors.

Amin Karimi-MoghadamDivision of Genetics, Department of Biology, Faculty of Science, University of Isfahan, Isfahan, Iran.
Saeid CharsoueiDepartment of Neurology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Benjamin BellHuman Genetics & Genomic Medicine, Faculty of Medicine, Southampton General Hospital, University of Southampton, Southampton, UK.
Mohammad Reza JabalameliDivision of Genetics, Department of Biology, Faculty of Science, University of Isfahan, Isfahan, Iran. mjaf1d14@soton.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson disease (PD) is known as a common progressive neurodegenerative disease which is clinically diagnosed by the manifestation of numerous motor and nonmotor symptoms. PD is a genetically heterogeneous disorder with both familial and sporadic forms. To date, researches in the field of Parkinsonism have identified 23 genes or loci linked to rare monogenic familial forms of PD with Mendelian inheritance. Biochemical studies revealed that the products of these genes usually play key roles in the proper protein and mitochondrial quality control processes, as well as synaptic transmission and vesicular recycling pathways within neurons. Despite this, large number of patients affected with PD typically tends to show sporadic forms of disease with lack of a clear family history. Recent genome-wide association studies (GWAS) meta-analyses on the large sporadic PD case-control samples from European populations have identified over 12 genetic risk factors. However, the genetic etiology that underlies pathogenesis of PD is also discussed, since it remains unidentified in 40% of all PD-affected cases. Nowadays, with the emergence of new genetic techniques, international PD genomics consortiums and public online resources such as PDGene, there are many hopes that future large-scale genetics projects provide further insights into the genetic etiology of PD and improve diagnostic accuracy and therapeutic clinical trial designs.

Indexed as

AnimalsAutophagyGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMitochondriaMutationParkinson DiseaseAutophagyGWAS meta-analysisMitochondrial dysfunctionNeurodegenerationOxidative stressParkinson disease

Identifiers

PMID29700661
PMCPMC6061130

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Registered trials

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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.