ArticlePloS one2011
Genetic cross-interaction between APOE and PRNP in sporadic Alzheimer's and Creutzfeldt-Jakob diseases.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 37 citations in OpenAlex.
- Metabolic Overlap between Alzheimer's Disease and Metabolic Syndrome Identifies theInternational journal of molecular sciences · 2023Article
- Cross interactions between Apolipoprotein E and amyloid proteins in neurodegenerative diseases.Computational and structural biotechnology journal · 2023Review
- Multiomics Identification of Potential Targets for Alzheimer Disease and Antrocin as a Therapeutic Candidate.Pharmaceutics · 2021Article
- Genetic Risk Factors of Creutzfeldt-Jakob Disease in the Population of Newborns in Slovakia.Pathogens (Basel, Switzerland) · 2021Article
- Longitudinal clinical, neuropsychological, and neuroimaging characterization of a kindred with a 12-octapeptide repeat insertion inNeurocase · 2020Article
- Sporadic Creutzfeldt-Jakob Disease and Other Proteinopathies in Comorbidity.Frontiers in neurology · 2020Article
- The characterization of AD/PART co-pathology in CJD suggests independent pathogenic mechanisms and no cross-seeding between misfolded Aβ and prion proteins.Acta neuropathologica communications · 2019Article
- Prion Protein PRNP: A New Player in Innate Immunity? The Aβ Connection.Journal of Alzheimer's disease reports · 2017Article
- CSF Tau proteins reduce misdiagnosis of sporadic Creutzfeldt-Jakob disease suspected cases with inconclusive 14-3-3 result.Journal of neurology · 2016Article
- Biomarkers for sporadic Creutzfeldt-Jakob disease.Annals of clinical and translational neurology · 2016Review
- Drivers: A Biologically Contextualized, Cross-Inferential View of the Epidemiology of Neurodegenerative Disorders.Journal of Alzheimer's disease : JAD · 2016Article
- Lack of association of the M129V polymorphism of the PRNP gene with pseudoexfoliation syndrome.Clinical ophthalmology (Auckland, N.Z.) · 2016Article
- Analyses of the mitochondrial mutations in the Chinese patients with sporadic Creutzfeldt-Jakob disease.European journal of human genetics : EJHG · 2015Article
- Additional mechanisms conferring genetic susceptibility to Alzheimer's disease.Frontiers in cellular neuroscience · 2015Review
- Genetic studies in human prion diseases.Journal of Korean medical science · 2014Review
- The cellular prion protein traps Alzheimer's Aβ in an oligomeric form and disassembles amyloid fibers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Specific profile of tau isoforms in argyrophylic grain disease.Journal of experimental neuroscience · 2013Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) and Creutzfeldt-Jakob disease (CJD) represent two distinct clinical entities belonging to a wider group, generically named as conformational disorders that share common pathophysiologic mechanisms. It is well-established that the APOE ε4 allele and homozygosity at polymorphic codon 129 in the PRNP gene are the major genetic risk factors for AD and human prion diseases, respectively. However, the roles of PRNP in AD, and APOE in CJD are controversial. In this work, we investigated for the first time, APOE and PRNP genotypes simultaneously in 474 AD and 175 sporadic CJD (sCJD) patients compared to a common control population of 335 subjects. Differences in genotype distribution between patients and control subjects were studied by logistic regression analysis using age and gender as covariates. The effect size of risk association and synergy factors were calculated using the logistic odds ratio estimates. Our data confirmed that the presence of APOE ε4 allele is associated with a higher risk of developing AD, while homozygosity at PRNP gene constitutes a risk for sCJD. Opposite, we found no association for PRNP with AD, nor for APOE with sCJD. Interestingly, when AD and sCJD patients were stratified according to their respective main risk genes (APOE for AD, and PRNP for sCJD), we found statistically significant associations for the other gene in those strata at higher previous risk. Synergy factor analysis showed a synergistic age-dependent interaction between APOE and PRNP in both AD (SF = 3.59, p = 0.027), and sCJD (SF = 7.26, p = 0.005). We propose that this statistical epistasis can partially explain divergent data from different association studies. Moreover, these results suggest that the genetic interaction between APOE and PRNP may have a biological correlate that is indicative of shared neurodegenerative pathways involved in AD and sCJD.
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.