ArticlePloS one2012
A common BACE1 polymorphism is a risk factor for sporadic Creutzfeldt-Jakob disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Biology, function and structure of the calcium homeostasis modulator family.The Journal of physiology · 2025Review
- Drivers: A Biologically Contextualized, Cross-Inferential View of the Epidemiology of Neurodegenerative Disorders.Journal of Alzheimer's disease : JAD · 2016Article
- Etiologic Framework for the Study of Neurodegenerative Disorders as Well as Vascular and Metabolic Comorbidities on the Grounds of Shared Epidemiologic and Biologic Features.Frontiers in aging neuroscience · 2016Article
- Multifaceted Role of Sialylation in Prion Diseases.Frontiers in neuroscience · 2016Review
- Analyses of the mitochondrial mutations in the Chinese patients with sporadic Creutzfeldt-Jakob disease.European journal of human genetics : EJHG · 2015Article
- Association of a BACE1 Gene Polymorphism with Parkinson's Disease in a Norwegian Population.Parkinson's disease · 2015Article
- Genetic studies in human prion diseases.Journal of Korean medical science · 2014Review
- RARB and STMN2 polymorphisms are not associated with sporadic Creutzfeldt-Jakob disease (CJD) in the Korean population.Molecular biology reports · 2014Article
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Authors and funding
12 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The β site APP cleaving enzyme 1 (BACE1) is the rate-limiting β-secretase enzyme in the amyloidogenic processing of APP and Aβ formation, and therefore it has a prominent role in Alzheimer's disease (AD) pathology. Recent evidence suggests that the prion protein (PrP) interacts directly with BACE1 regulating its β-secretase activity. Moreover, PrP has been proposed as the cellular receptor involved in the impairment of synaptic plasticity and toxicity caused by Aβ oligomers. Provided that common pathophysiologic mechanisms are shared by Alzheimer's and Creutzfeldt-Jakob (CJD) diseases, we investigated for the first time to the best of our knowledge a possible association of a common synonymous BACE1 polymorphism (rs638405) with sporadic CJD (sCJD). Our results indicate that BACE1 C-allele is associated with an increased risk for developing sCJD, mainly in PRNP M129M homozygous subjects with early onset. These results extend the very short list of genes (other than PRNP) involved in the development of human prion diseases; and support the notion that similar to AD, in sCJD several loci may contribute with modest overall effects to disease risk. These findings underscore the interplay in both pathologies of APP, Aβ oligomers, ApoE, PrP and BACE1, and suggest that aging and perhaps vascular risk factors may modulate disease pathologies in part through these key players.
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