ReviewParkinson's disease2018
The Association between E326K of
Review in Parkinson's disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- GBA1 Variants with Unknown Classification Are Modest Contributors to Parkinson's Disease Susceptibility.Movement disorders : official journal of the Movement Disorder Society · 2026Pooled it
- E326KJournal of Parkinson's disease · 2026Article
- Classification of GBA1 variants and their impact on Parkinson's disease: an in silico score analysis.NPJ Parkinson's disease · 2025Article
- Stearoyl-CoA desaturase inhibition normalizes brain lipid saturation, α-synuclein homeostasis, and motor function in mutant Gba1-Parkinson mice.JCI insight · 2025Article
- A PheWAS approach to identify associations of GBA1 variants with comprehensive phenotypes beyond neurological diseases.NPJ Parkinson's disease · 2025Article
- Relevance of genetic testing in the gene-targeted trial era: the Rostock Parkinson's disease study.Brain : a journal of neurology · 2024Observational
- Classification of GBA1 Variants in Parkinson's Disease: The GBA1-PD Browser.Movement disorders : official journal of the Movement Disorder Society · 2023Review
- Artificial intelligence-based clustering and characterization of Parkinson's disease trajectories.Scientific reports · 2023Article
- From cradle to grave: neurogenesis, neuroregeneration and neurodegeneration in Alzheimer's and Parkinson's diseases.Neural regeneration research · 2022Review
- Tools for communicating risk for Parkinson's disease.NPJ Parkinson's disease · 2022Article
- Lack of full sequencing GBA1 studies for patients with Parkinson's disease in Latin America.NPJ Parkinson's disease · 2022Article
- Genome Sequencing in the Parkinson Disease Clinic.Neurology. Genetics · 2022Article
- Article
- Review
- GBA1 and The Immune System: A Potential Role in Parkinson's Disease?Journal of Parkinson's disease · 2022Review
- A randomized single and multiple ascending dose study in healthy volunteers of LTI-291, a centrally penetrant glucocerebrosidase activator.British journal of clinical pharmacology · 2021Article
- Next-generation sequencing for constitutional variants in the clinical laboratory, 2021 revision: a technical standard of the American College of Medical Genetics and Genomics (ACMG).Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Experience in Genetic Counseling forMovement disorders clinical practice · 2021Article
- A Large-Scale Full GBA1 Gene Screening in Parkinson's Disease in the Netherlands.Movement disorders : official journal of the Movement Disorder Society · 2020Article
- Common Variants Coregulate Expression of GBA and Modifier Genes to Delay Parkinson's Disease Onset.Movement disorders : official journal of the Movement Disorder Society · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is reported that both the homozygous and heterozygous states of GBA mutations which are the causes of Gaucher disease (GD) are linked to the risk of PD. However, the GBA variant p.E326K (c.1093G > A, rs2230288), which does not result in GD in homozygous carriers, has triggered debate among experts studying Parkinson's disease (PD). In order to determine if the E326K variant of GBA is associated with the risk of PD, a standard meta-analysis was conducted by searching and screening publications, data extraction, and statistical analysis. Finally, a total of 15 publications, containing 5,908 PD patients and 5,605 controls, were included in this analysis. The pooled OR of the E326K genotype analysis was 1.99 (95% CI: 1.57-2.51). The minor allele frequencies of E326K for PD patients and controls were 1.67% and 1.03%, respectively. The pooled OR for the minor allele A was 1.99 (95% CI: 1.58-2.50). According to the subgroup analysis, we found that the significant differences between PD patients and controls for both genotype and allele of E326K also exist in Asians and Caucasians, respectively. In this study, we found that E326K of GBA is associated with the risk of PD in total populations, Asians, and Caucasians, respectively. Further studies are needed to clarify the role of GBA in the pathogenesis of PD.
Identifiers
What OpenQuestion holds
Registered trials
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.