Evidence map›Paper›PMID 34871738›Full record

ReviewNeurobiology of disease2022

Multi-omic insights into Parkinson's Disease: From genetic associations to functional mechanisms.

Brian M Schilder, Elisa Navarro, Towfique Raj

Abstract readReview
In one paragraph

Review in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Semi-supervised ensemble learning with interval type-2 fuzzy-rough sets for Parkinson's disease prediction from multi-omics.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Common genetic risk for Parkinson's disease and dysfunction of the endo-lysosomal system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  14. Article
  15. Insights into Neurodegeneration in Parkinson's Disease from Single-Cell and Spatial Genomics.Movement disorders : official journal of the Movement Disorder Society · 2023
    Article
  16. Article
  17. Article
  18. 3α,7-Dihydroxy-14(13→12)Biomolecules · 2022
    Article
  19. Review
  20. The immunology of Parkinson's disease.Seminars in immunopathology · 2022
    Review
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

3 authors.

Brian M SchilderNash Family Department of Neuroscience & Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Ronald M. Loeb Center for Alzheimer's disease, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Icahn Institute for Data Science and Genomic Technology, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Estelle and Daniel Maggin Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Department of Brain Sciences, Faculty of Medicine, Imperial College London, London, United Kingdom; UK Dementia Research Institute at Imperial College London, London, United Kingdom. Electronic address: brian_schilder@alumni.brown.edu.
Elisa NavarroNash Family Department of Neuroscience & Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Ronald M. Loeb Center for Alzheimer's disease, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Icahn Institute for Data Science and Genomic Technology, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Estelle and Daniel Maggin Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Sección Departamental de Bioquímica y Biología Molecular, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Towfique RajNash Family Department of Neuroscience & Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Ronald M. Loeb Center for Alzheimer's disease, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Icahn Institute for Data Science and Genomic Technology, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Estelle and Daniel Maggin Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, United States. Electronic address: towfique.raj@mssm.edu.

Funding

Research Education ComponentP30AG066514 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI NIKOLAOS K ROBAKIS · 2020 to 2026
$31.0M
Dissecting Oligogenic Biomarkers in Ashkenazi Jews with Parkinson DiseaseU01NS107016 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI OZELIUS, LAURIE J., SAUNDERS-PULLMAN, RACHEL · 2019 to 2023
$6.6M
The role of peripheral myeloid cells in Alzheimers diseaseR01AG054005 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI RAJ, TOWFIQUE · 2017 to 2021
$4.1M
The Role of Myeloid Cells in Parkinson's DiseaseR01NS116006 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Towfique Raj · 2021 to 2026
$4.0M
Identifying genetic and transcriptomic drivers of Parkinson's disease progressionU01NS120256 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI RAJ, TOWFIQUE · 2020 to 2020
$507k
Medical Research CouncilNIA NIH HHS P30 AG066514NIA NIH HHS R01 AG054005NINDS NIH HHS R01 NS116006NINDS NIH HHS U01 NS107016NINDS NIH HHS U01 NS120256
6 · The paper itself

Abstract

Genome-Wide Association Studies (GWAS) have elucidated the genetic components of Parkinson's Disease (PD). However, because the vast majority of GWAS association signals fall within non-coding regions, translating these results into an interpretable, mechanistic understanding of the disease etiology remains a major challenge in the field. In this review, we provide an overview of the approaches to prioritize putative causal variants and genes as well as summarise the primary findings of previous studies. We then discuss recent efforts to integrate multi-omics data to identify likely pathogenic cell types and biological pathways implicated in PD pathogenesis. We have compiled full summary statistics of cell-type, tissue, and phentoype enrichment analyses from multiple studies of PD GWAS and provided them in a standardized format as a resource for the research community (https://github.com/RajLabMSSM/PD_omics_review). Finally, we discuss the experimental, computational, and conceptual advances that will be necessary to fully elucidate the effects of functional variants and genes on cellular dysregulation and disease risk.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideQuantitative Trait LociGenome-Wide Association StudyGenomicsHumansParkinson DiseaseGenome-wide association study (GWAS)Meta-analysisMulti-omicsNeurodegenerationParkinson's DiseasePhenomeQuantitative trait loci (QTL)

Identifiers

PMID34871738
PMCPMC10101343

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.