Evidence map›Paper›PMID 31518392›Full record

ReviewHuman molecular genetics2019

Progress in the genetic analysis of Parkinson's disease.

Andrew Singleton, John Hardy

Abstract readReview
In one paragraph

Review in Human molecular genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–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

23 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. The Endotoxin Hypothesis of Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2023
    Review
  9. Parkinson's disease therapy: what lies ahead?Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Targeted Molecular Therapeutics for Parkinson's Disease: A Role for Antisense Oligonucleotides?Movement disorders : official journal of the Movement Disorder Society · 2022
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Therapeutic Potential ofParkinson's disease · 2021
    Review
  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.

Andrew SingletonLaboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA.
John HardyDementia Research Institute and Department of Neurodegeneration and Reta Lila Weston Laboratories, Institute of Neurology, London, UK.

Funding

Medical Research Council G0701075Medical Research Council G0901254Medical Research Council MR/K01417X/1Medical Research Council MR/N026004/1Parkinson's UK G-0907Wellcome Trust 202903/Z/16/Z
6 · The paper itself

Abstract

The pace of genetic discovery in complex disease has accelerated exponentially over the last decade. Our fund of knowledge of the foundational genetics in disease has never been as great. There is a clear path forward to the resolution of the genetic architecture toward a point at which we will saturate the biological understanding of disease through genetics. This understanding continues to provide fundamental insights into disease biology and, with the advent of new data and methodologies, the path from gene to function is becoming clearer and cleaner. In this opinion piece, we discuss progress in the genetics of Parkinson disease. We explore what genetics has revealed thus far in the context of disease biology. We highlight mitophagy/autophagy, dopamine metabolism and the adaptive immune system. We try and link these findings together to give a holistic view of pathogenesis with the underlying theme that disease pathogenesis relates to a failure of damage response pathways. In the 1990s, Parkinson's disease was regarded a non-genetic disorder. Since that time, however, a huge number of Mendelian loci and risk loci have been identified by positional cloning and by genome-wide association studies. In this review, it is not our intent to list each gene and locus and review their identification [Hernandez, D.G., Reed, X. and Singleton, A.B. (2016) Genetics in Parkinson disease: Mendelian versus non-Mendelian inheritance. J. Neurochem., 139 Suppl 1, 59-74] but rather to outline the pathogenetic mechanisms that these analyses are revealing and then, given the large number of loci already identified, to lay out what we hope future analyses may help us understand, both in terms of disease mechanisms and for risk prediction for the syndrome.

Indexed as

AutophagyDopamineEndodeoxyribonucleasesGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMitophagyOxidative StressParkinson DiseasePhenotypeRisk FactorsUbiquitin-Protein LigasesDNASE1L3 protein, humanDopamineEndodeoxyribonucleasesparkin proteinUbiquitin-Protein Ligases

Identifiers

PMID31518392
PMCPMC6872433

What OpenQuestion holds

Textmetadata
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.