SynthesisJAMA neurology2013
Analysis of genome-wide association studies of Alzheimer disease and of Parkinson disease to determine if these 2 diseases share a common genetic risk.
Synthesis in JAMA neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 62 citations in OpenAlex.
- CardiacClinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Family History of AD/Dementia, Polygenic Risk Score for AD, and Parkinson's Disease.Movement disorders clinical practice · 2023Article
- Local genetic correlations exist among neurodegenerative and neuropsychiatric diseases.NPJ Parkinson's disease · 2023Article
- Dissecting the limited genetic overlap of Parkinson's and Alzheimer's disease.Annals of clinical and translational neurology · 2022Article
- Genome-wide association studies for Alzheimer's disease: bigger is not always better.Brain communications · 2022Review
- Polygenic Score Models for Alzheimer's Disease: From Research to Clinical Applications.Frontiers in neuroscience · 2021Review
- Polygenic risk and pleiotropy in neurodegenerative diseases.Neurobiology of disease · 2020Review
- The multiplex model of the genetics of Alzheimer's disease.Nature neuroscience · 2020Review
- Gene-Editing Technologies Paired With Viral Vectors for Translational Research Into Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2020Article
- Neuropathology and pathogenesis of extrapyramidal movement disorders: a critical update-I. Hypokinetic-rigid movement disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Dementia with Lewy bodies: an update and outlook.Molecular neurodegeneration · 2019Review
- Converging pathways in neurodegeneration, from genetics to mechanisms.Nature neuroscience · 2018Review
- The Genetics of Dementia with Lewy Bodies: Current Understanding and Future Directions.Current neurology and neuroscience reports · 2018Review
- Nucleolar Stress: hallmarks, sensing mechanism and diseases.Cell stress · 2018Review
- Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study.The Lancet. Neurology · 2018Article
- FOLD: a method to optimize power in meta-analysis of genetic association studies with overlapping subjects.Bioinformatics (Oxford, England) · 2017Article
- Similarity and Differences in Inflammation-Related Characteristics of the Peripheral Immune System of Patients with Parkinson's and Alzheimer's Diseases.International journal of molecular sciences · 2017Review
- Analysis of neurodegenerative Mendelian genes in clinically diagnosed Alzheimer Disease.PLoS genetics · 2017Article
- Increasing the power of meta-analysis of genome-wide association studies to detect heterogeneous effects.Bioinformatics (Oxford, England) · 2017Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors at 1 institution in 1 country.
Funding
Abstract
importanceDespite Alzheimer disease (AD) and Parkinson disease (PD) being clinically distinct entities, there is a possibility of a pathological overlap, with some genome-wide association (GWA) studies suggesting that the 2 diseases represent a biological continuum. The application of GWA studies to idiopathic forms of AD and PD have identified a number of loci that contain genetic variants that increase the risk of these disorders.
objectiveTo assess the genetic overlap between PD and AD by testing for the presence of potentially pleiotropic loci in 2 recent GWA studies of PD and AD.
designCombined GWA analysis.
settingData sets from the United Kingdom, Germany, France, and the United States.
participantsThousands of patients with AD or PD and their controls. MAIN OUTCOMES AND MEASURES: Meta-analysis of GWA studies of AD and PD.
methodsTo identify evidence for potentially pleiotropic alleles that increased the risk for both PD and AD, we performed a combined PD-AD meta-analysis and compared the results with those obtained in the primary GWA studies.We also tested for a net effect of potentially polygenic alleles that were shared by both disorders by performing a polygenic score analysis. Finally, we also performed a gene-based association analysis that was aimed at detecting genes that harbor multiple disease-causing single-nucleotide polymorphisms, some of which confer a risk of PD and some a risk of AD.
resultsDetailed interrogation of the single-nucleotide polymorphism, polygenic, and gene-based analyses resulted in no significant evidence that supported the presence of loci that increase the risk of both PD and AD. CONCLUSIONS AND RELEVANCE: Our findings therefore imply that loci that increase the risk of both PD and AD are not widespread and that the pathological overlap could instead be “downstream” of the primary susceptibility genes that increase the risk of each disease.
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.