MétaCan
Menu
Back to cohort
Record W4361190782 · doi:10.1093/brain/awad101

Seed amplification and neurodegeneration marker trajectories in individuals at risk of prion disease

2023· article· en· W4361190782 on OpenAlexaff
Tze How Mok, Akın Nihat, Nour K. Majbour, Danielle Sequeira, Leah Holm-Mercer, Thomas Coysh, Lee Darwent, Mark Batchelor, Bradley R. Groveman, C. Orr, Andrew G. Hughson, Amanda Heslegrave, Rhiannon Laban, Elena Veleva, Ross W. Paterson, Ashvini Keshavan, Jonathan M. Schott, Imogen J. Swift, Carolin Heller, Jonathan D. Rohrer, Alexander Gerhard, Christopher Butler, James B. Rowe, Mario Masellis, Miles Chapman, Michael P. Lunn, Jan Bieschke, Graham S. Jackson, Henrik Zetterberg, Byron Caughey, Peter Rudge, John Collinge, Simon Mead

Bibliographic record

VenueBrain · 2023
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicPrion Diseases and Protein Misfolding
Canadian institutionsHealth Sciences CentreUniversity of TorontoSunnybrook Health Science Centre
FundersNational Institutes of HealthUK Dementia Research InstituteVetenskapsrådetKnut och Alice Wallenbergs StiftelseHjärnfondenUniversity College LondonNHLBI Division of Intramural ResearchDepartment of Health and Social CareNational Institute for Health and Care ResearchWellcome TrustAlzheimer's SocietyFamiljen Erling-Perssons StiftelseStiftelsen för Gamla TjänarinnorNIHR Cambridge Biomedical Research CentreUniversity College London Hospitals NHS Foundation TrustEuropean CommissionDivision of Intramural Research, National Institute of Allergy and Infectious DiseasesNational Institute of Allergy and Infectious DiseasesMedical Research CouncilNational Institute on Handicapped ResearchAlzheimer's Drug Discovery Foundation
KeywordsNeurodegenerationBiomarkerMedicineDiseaseAsymptomaticPathologyVirologyImmunologyInternal medicineOncologyBiologyGenetics

Abstract

fetched live from OpenAlex

Human prion diseases are remarkable for long incubation times followed typically by rapid clinical decline. Seed amplification assays and neurodegeneration biofluid biomarkers are remarkably useful in the clinical phase, but their potential to predict clinical onset in healthy people remains unclear. This is relevant not only to the design of preventive strategies in those at-risk of prion diseases, but more broadly, because prion-like mechanisms are thought to underpin many neurodegenerative disorders. Here, we report the accrual of a longitudinal biofluid resource in patients, controls and healthy people at risk of prion diseases, to which ultrasensitive techniques such as real-time quaking-induced conversion (RT-QuIC) and single molecule array (Simoa) digital immunoassays were applied for preclinical biomarker discovery. We studied 648 CSF and plasma samples, including 16 people who had samples taken when healthy but later developed inherited prion disease (IPD) ('converters'; range from 9.9 prior to, and 7.4 years after onset). Symptomatic IPD CSF samples were screened by RT-QuIC assay variations, before testing the entire collection of at-risk samples using the most sensitive assay. Glial fibrillary acidic protein (GFAP), neurofilament light (NfL), tau and UCH-L1 levels were measured in plasma and CSF. Second generation (IQ-CSF) RT-QuIC proved 100% sensitive and specific for sporadic Creutzfeldt-Jakob disease (CJD), iatrogenic and familial CJD phenotypes, and subsequently detected seeding activity in four presymptomatic CSF samples from three E200K carriers; one converted in under 2 months while two remain asymptomatic after at least 3 years' follow-up. A bespoke HuPrP P102L RT-QuIC showed partial sensitivity for P102L disease. No compatible RT-QuIC assay was discovered for classical 6-OPRI, A117V and D178N, and these at-risk samples tested negative with bank vole RT-QuIC. Plasma GFAP and NfL, and CSF NfL levels emerged as proximity markers of neurodegeneration in the typically slow IPDs (e.g. P102L), with significant differences in mean values segregating healthy control from IPD carriers (within 2 years to onset) and symptomatic IPD cohorts; plasma GFAP appears to change before NfL, and before clinical conversion. In conclusion, we show distinct biomarker trajectories in fast and slow IPDs. Specifically, we identify several years of presymptomatic seeding positivity in E200K, a new proximity marker (plasma GFAP) and sequential neurodegenerative marker evolution (plasma GFAP followed by NfL) in slow IPDs. We suggest a new preclinical staging system featuring clinical, seeding and neurodegeneration aspects, for validation with larger prion at-risk cohorts, and with potential application to other neurodegenerative proteopathies.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.400
Threshold uncertainty score0.247

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.010
GPT teacher head0.246
Teacher spread0.236 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations45
Published2023
Admission routes1
Has abstractyes

Explore more

Same venueBrainSame topicPrion Diseases and Protein MisfoldingFrench-language works237,207