ArticleAnnals of human genetics2008
A genome-wide scan in an Amish pedigree with parkinsonism.
Article in Annals of human genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed.
- A longitudinal study of age-related traits and cognitive function: The Collaborative Amish Aging and Memory Project (CAAMP).medRxiv : the preprint server for health sciences · 2026Article
- Genomewide Association Studies of LRRK2 Modifiers of Parkinson's Disease.Annals of neurology · 2021Article
- The GGLEAM Study: Understanding Glaucoma in the Ohio Amish.International journal of environmental research and public health · 2021Article
- Parkinson's Disease-Related Motor and Nonmotor Symptoms in the Lancaster Amish.Neuroepidemiology · 2020Article
- Parkinson disease loci in the mid-western Amish.Human genetics · 2013Article
- Article
- A genome-wide linkage screen in the Amish with Parkinson disease points to chromosome 6.Annals of human genetics · 2011Article
- PedHunter 2.0 and its usage to characterize the founder structure of the Old Order Amish of Lancaster County.BMC medical genetics · 2010Article
- Genome-wide linkage screen in familial Parkinson disease identifies loci on chromosomes 3 and 18.American journal of human genetics · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
The identification of familial Parkinson Disease (PD) genes is yielding important molecular pathogenetic insights. In an effort to identify additional PD genes, we studied an eight generation Amish pedigree with apparent autosomal dominant parkinsonism with incomplete penetrance. Phenotypic variability ranged from idiopathic PD to progressive supranuclear palsy (PSP), with the average age at onset 53 years (range of 39 to 74 years). We identified markers on chromosome 3 and 7 that were significant at a genome-wide level by parametric and nonparametric criteria, lod > 3 and non-parametric P-value < 0.10, respectively. We also identified markers on chromosomes 10 and 22 with lod > 3. These data suggest that parkinsonism in this pedigree is genetically complex, with contributions from several loci.
Indexed as
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.