Trial reportPloS one2015
Parkinson's Disease in Saudi Patients: A Genetic Study.
Trial report in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- Breaking barriers and fighting inequality in Parkinson's disease care: Personal reflections of movement disorders clinicians.Journal of Parkinson's disease · 2026Article
- Dynamic structural profiling of PINK1 mutations (T313M and L347P) reveals a vital molecular perturbation namely phospho-Serine 65 ubiquitin recognition point in mitophagy mediated autosomal recessive Parkinson's disease (ARPD).Frontiers in molecular neuroscience · 2026Article
- Absence of theFrontiers in aging neuroscience · 2025Article
- Review
- First Two-Year Observational Exploratory Real Life Clinical Phenotyping, and Societal Impact Study of Parkinson's Disease in Emiratis and Expatriate Population of United Arab Emirates 2019-2021: The EmPark Study.Journal of personalized medicine · 2022Article
- LCIG in treatment of non-motor symptoms in advanced Parkinson's disease: Review of literature.Brain and behavior · 2020Review
- Parkinson's Disease in the Middle East, North Africa, and South Asia: Consensus from the International Parkinson and Movement Disorder Society Task Force for the Middle East.Journal of Parkinson's disease · 2020Article
- Integrated Analysis of Whole Exome Sequencing and Copy Number Evaluation in Parkinson's Disease.Scientific reports · 2019Article
- Novel Compound HeterozygousParkinson's disease · 2019Article
- Parkinson's Disease: Patients' Knowledge, Attitudes, and Interest in Genetic Counseling.Journal of genetic counseling · 2018Article
- Copy number variability in Parkinson's disease: assembling the puzzle through a systems biology approach.Human genetics · 2017Review
- Evidence for prehistoric origins of the G2019S mutation in the North African Berber population.PloS one · 2017Article
- Clinical heterogeneity of PLA2G6-related Parkinsonism: analysis of two Saudi families.BMC research notes · 2016Article
- Public knowledge and awareness about Parkinson's disease in Saudi Arabia.Journal of family medicine and primary careArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is one of the major causes of parkinsonism syndrome. Its characteristic motor symptoms are attributable to dopaminergic neurons loss in the midbrain. Genetic advances have highlighted underlying molecular mechanisms and provided clues to potential therapies. However, most of the studies focusing on the genetic component of PD have been performed on American, European and Asian populations, whereas Arab populations (excluding North African Arabs), particularly Saudis remain to be explored. Here we investigated the genetic causes of PD in Saudis by recruiting 98 PD-cases (sporadic and familial) and screening them for potential pathogenic mutations in PD-established genes; SNCA, PARKIN, PINK1, PARK7/DJ1, LRRK2 and other PD-associated genes using direct sequencing. To our surprise, the screening revealed only three pathogenic point mutations; two in PINK1 and one in PARKIN. In addition to mutational analysis, CNV and cDNA analysis was performed on a subset of patients. Exon/intron dosage alterations in PARKIN were detected and confirmed in 2 cases. Our study suggests that mutations in the ORF of the screened genes are not a common cause of PD in Saudi population; however, these findings by no means exclude the possibility that other genetic events such as gene expression/dosage alteration may be more common nor does it eliminate the possibility of the involvement of novel genes.
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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.