ArticleActa neuropathologica communications2023
Sporadic Creutzfeldt-Jakob disease infected human cerebral organoids retain the original human brain subtype features following transmission to humanized transgenic mice.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Mapping the Cerebral Organoid Landscape: A Systematic Review of Preclinical 3D Models in Neuroscience.Advanced healthcare materials · 2026Pooled it
- Distinct neuronal alterations distinguish two subtypes of sporadic Creutzfeldt-Jakob disease with shared dysfunctional pathways.The Journal of clinical investigation · 2026Article
- Prion-induced ferroptosis is facilitated by RAC3.Nature communications · 2025Article
- Prion and "Prion-Like" Detection: From Conventional Methods to Microfluidics or Lab-on-Chip Platforms to Monitor Seeding and Spreading of Misfolded Proteins.Sub-cellular biochemistry · 2025Review
- Infecting human brain organoids with FFI or sCJD preserves prion traits regardless of host genotype.NPJ dementia · 2025Article
- Tracking Prions by RT-QuIC: An Update.Sub-cellular biochemistry · 2025Review
- Limbic system synaptic dysfunctions associated with prion disease onset.Acta neuropathologica communications · 2024Article
- Lack of Transmission of Chronic Wasting Disease Prions to Human Cerebral Organoids.Emerging infectious diseases · 2024Article
- Advanced Cellular Models for Rare Disease Study: Exploring Neural, Muscle and Skeletal Organoids.International journal of molecular sciences · 2024Review
- Sodium hypochlorite inactivation of human CJD prions.PloS one · 2024Article
- Neural cell engraftment therapy for sporadic Creutzfeldt-Jakob disease restores neuroelectrophysiological parameters in a cerebral organoid model.Stem cell research & therapy · 2023Article
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8 authors at 2 institutions in 2 countries.
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Abstract
Human cerebral organoids (COs) are three-dimensional self-organizing cultures of cerebral brain tissue differentiated from induced pluripotent stem cells. We have recently shown that COs are susceptible to infection with different subtypes of Creutzfeldt-Jakob disease (CJD) prions, which in humans cause different manifestations of the disease. The ability to study live human brain tissue infected with different CJD subtypes opens a wide array of possibilities from differentiating mechanisms of cell death and identifying neuronal selective vulnerabilities to testing therapeutics. However, the question remained as to whether the prions generated in the CO model truly represent those in the infecting inoculum. Mouse models expressing human prion protein are commonly used to characterize human prion disease as they reproduce many of the molecular and clinical phenotypes associated with CJD subtypes. We therefore inoculated these mice with COs that had been infected with two CJD subtypes (MV1 and MV2) to see if the original subtype characteristics (referred to as strains once transmitted into a model organism) of the infecting prions were maintained in the COs when compared with the original human brain inocula. We found that disease characteristics caused by the molecular subtype of the disease associated prion protein were similar in mice inoculated with either CO derived material or human brain material, demonstrating that the disease associated prions generated in COs shared strain characteristics with those in humans. As the first and only in vitro model of human neurodegenerative disease that can faithfully reproduce different subtypes of prion disease, these findings support the use of the CO model for investigating human prion diseases and their subtypes.
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