ArticleJournal of neurology2005
A genome wide linkage disequilibrium screen in Parkinson's disease.
Article in Journal of neurology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Parkinson disease loci in the mid-western Amish.Human genetics · 2013Article
- Genome-wide linkage screen in familial Parkinson disease identifies loci on chromosomes 3 and 18.American journal of human genetics · 2009Article
- Commentary on "A genome wide linkage disequilibrium screen in Parkinson's disease" by Foltynie et al. in J Neurol (2005) 252:597-602.Journal of neurology · 2005Article
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Authors and funding
13 authors.
Funding
Abstract
Whole genome screening is increasingly used to identify genetic risk factors for complex diseases. In this study, a genome wide linkage disequilibrium (LD) screen was performed in a cohort of Parkinson's disease (PD) patients from the UK (n = 195) using pooled DNA to facilitate efficient genotyping of 5546 microsatellite markers. Allele frequencies were compared with those found in 2 previously typed disease free control populations, and the most interesting markers were selected for multiple repeat testing among the 3 pools. Markers were then individually genotyped in our original PD cohort and one of the original control groups, and independently in a second cohort of UK PD patients (n = 179), and additional controls. Using this 2-stage approach, we have been unable to find evidence for consistent association of any markers with sporadic PD. Subgroup analysis of the most promising marker shows some evidence that microsatellite marker D1S2886 is associated with familial forms of the disease.
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