ArticleActa neuropathologica communications2019
The characterization of AD/PART co-pathology in CJD suggests independent pathogenic mechanisms and no cross-seeding between misfolded Aβ and prion proteins.
Article in Acta neuropathologica communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prion disease mimicking rapidly progressive Alzheimer disease: case series and systematic review.Journal of neurology · 2026Pooled it
- A Diagnostic Pitfall in the Era of Amyloid-Targeting Therapy: Creutzfeldt-Jakob Disease Masquerading as Biologically Defined Alzheimer's Disease.Psychogeriatrics : the official journal of the Japanese Psychogeriatric Society · 2026Article
- The Bayesian approach for real-world implementation of plasma p-tau217 in tertiary care memory clinics in Thailand.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Cerebrospinal fluid p-tau181, 217, and 231 in definite Creutzfeldt-Jakob disease with and without concomitant pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Striking intraneuronal neurofilament inclusions restricted to the locus coeruleus in a patient with Creutzfeldt-Jakob disease.Free neuropathology · 2024Article
- An Atypical Case of Creutzfeldt-Jakob Syndrome Presenting with Cacosmia and Amyloid Positivity.Journal of Alzheimer's disease reports · 2024Article
- IgLON5 autoimmunity in a patient with Creutzfeldt-Jakob disease: case report and review of literature.Frontiers in neurology · 2024Article
- Metabolic Brain Changes Can Predict the Underlying Pathology in Neurodegenerative Brain Disorders: A Case Report of Sporadic Creutzfeldt-Jakob Disease with Concomitant Parkinson's Disease.International journal of molecular sciences · 2023Article
- Cross interactions between Apolipoprotein E and amyloid proteins in neurodegenerative diseases.Computational and structural biotechnology journal · 2023Review
- Sporadic Creutzfeldt-Jakob disease VM1: phenotypic and molecular characterization of a novel subtype of human prion disease.Acta neuropathologica communications · 2022Article
- Biomarkers Analysis and Clinical Manifestations in Comorbid Creutzfeldt-Jakob Disease: A Retrospective Study in 215 Autopsy Cases.Biomedicines · 2022Article
- Co-incidental C9orf72 expansion mutation-related frontotemporal lobar degeneration pathology and sporadic Creutzfeldt-Jakob disease.European journal of neurology · 2021Article
- Primary age-related tauopathy (PART) in the general autopsy setting: Not just a disease of the elderly.Brain pathology (Zurich, Switzerland) · 2021Article
- Extracellular Protein Aggregates Colocalization and Neuronal Dystrophy in Comorbid Alzheimer's and Creutzfeldt-Jakob Disease: A Micromorphological Pilot Study on 20 Brains.International journal of molecular sciences · 2021Article
- Understanding Creutzfeldt-Jackob disease from a viewpoint of amyloidogenic evolvability.Prion · 2020Review
- CSF SerpinA1 in Creutzfeldt-Jakob disease and frontotemporal lobar degeneration.Annals of clinical and translational neurology · 2020Article
- Prion protein codon 129 polymorphism in mild cognitive impairment and dementia: the Rotterdam Study.Brain communications · 2020Article
- Sporadic Creutzfeldt-Jakob Disease and Other Proteinopathies in Comorbidity.Frontiers in neurology · 2020Article
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Abstract
Current evidence indicating a role of the human prion protein (PrP) in amyloid-beta (Aβ) formation or a synergistic effect between Aβ and prion pathology remains controversial. Conflicting results also concern the frequency of the association between the two protein misfolding disorders and the issue of whether the apolipoprotein E gene (APOE) and the prion protein gene (PRNP), the major modifiers of Aβ- and PrP-related pathologies, also have a pathogenic role in other proteinopathies, including tau neurofibrillary degeneration. Here, we thoroughly characterized the Alzheimer's disease/primary age-related tauopathy (AD/PART) spectrum in a series of 450 cases with definite sporadic or genetic Creutzfeldt-Jakob disease (CJD). Moreover, we analyzed: (i) the effect of variables known to affect CJD pathogenesis and the co-occurring Aβ- and tau-related pathologies; (II) the influence of APOE genotype on CJD pathology, and (III) the effect of AD/PART co-pathology on the clinical CJD phenotype. AD/PART characterized 74% of CJD brains, with 53.3% and 8.2% showing low or intermediate-high levels of AD pathology, and 12.4 and 11.8% definite or possible PART. There was no significant correlation between variables affecting CJD (i.e., disease subtype, prion strain, PRNP genotype) and those defining the AD/PART spectrum (i.e., ABC score, Thal phase, prevalence of CAA and Braak stage), and no difference in the distribution of APOE ε4 and ε2 genotypes among CJD subtypes. Moreover, AD/PART co-pathology did not significantly affect the clinical presentation of typical CJD, except for a tendency to increase the frequency of cognitive symptoms. Altogether, the present results seem to exclude an increased prevalence AD/PART co-pathology in sporadic and genetic CJD, and indicate that largely independent pathogenic mechanisms drive AD/PART and CJD pathology even when they coexist in the same brain.
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