ArticleNature medicine2024
Iatrogenic Alzheimer's disease in recipients of cadaveric pituitary-derived growth hormone.
Article in Nature medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 85 citations in OpenAlex.
- Disease Progression in Iatrogenic Cerebral Amyloid Angiopathy.Neurology · 2026Article
- Article
- Article
- Evidence for progressive neurodegeneration in iatrogenic cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Prion-like transmission and propagation of human β-amyloid to the bank vole rodent model.Acta neuropathologica · 2026Article
- Strain-specific propagation of variant Creutzfeldt-Jakob disease prions in humanized neural cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- High-Level Alzheimer Disease Neuropathological Change Following Iatrogenic Exposure.JAMA neurology · 2026Article
- Proteomic signature of dementia risk in type 2 diabetes.Journal of advanced research · 2026Article
- Modelling human proteostasis and organelle homeostasis disorders in yeast and its application in drug discovery.FEMS yeast research · 2026Review
- Aerobic exercise combined with FK866 ameliorates Alzheimer's disease-like pathology in APP/PS1 mice with NAMPT abnormality.Frontiers in immunology · 2026Article
- One organelle to rule them all: enhancement of lysosomal activity as a therapeutic modality for protein misfolding neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- Alzheimer's disease: A comprehensive review of epidemiology, pathophysiology, diagnosis, and treatment.AIMS neuroscience · 2026Review
- Serum osteocalcin as a novel biomarker for differentiating growth hormone deficiency from idiopathic short stature.Frontiers in endocrinology · 2026Article
- Cognition, Diagnosis, and Treatment of Alzheimer's Disease: A Review.Recent patents on biotechnology · 2026Review
- Prions and protein aggregates as pathogens, self-propagating structures, biomarkers, and therapeutic targets.Microbiology and molecular biology reviews : MMBR · 2025Review
- The Determinant of Tau Spreading in Alzheimer's Disease: Dependent on Senile Plaque, Neural Circuits, or Spatial Proximity?International journal of molecular sciences · 2025Review
- Contrasting roles of autophagy in cellular prion infection.Autophagy · 2025Article
- Estimating future variant Creutzfeldt-Jakob disease cases in the UK: a cohort-based probabilistic model.The Lancet regional health. Europe · 2025Article
- Combined neocortical protein and morphological profiling of reactive microglia across Alzheimer's and Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2025Article
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized pathologically by amyloid-beta (Aβ) deposition in brain parenchyma and blood vessels (as cerebral amyloid angiopathy (CAA)) and by neurofibrillary tangles of hyperphosphorylated tau. Compelling genetic and biomarker evidence supports Aβ as the root cause of AD. We previously reported human transmission of Aβ pathology and CAA in relatively young adults who had died of iatrogenic Creutzfeldt-Jakob disease (iCJD) after childhood treatment with cadaver-derived pituitary growth hormone (c-hGH) contaminated with both CJD prions and Aβ seeds. This raised the possibility that c-hGH recipients who did not die from iCJD may eventually develop AD. Here we describe recipients who developed dementia and biomarker changes within the phenotypic spectrum of AD, suggesting that AD, like CJD, has environmentally acquired (iatrogenic) forms as well as late-onset sporadic and early-onset inherited forms. Although iatrogenic AD may be rare, and there is no suggestion that Aβ can be transmitted between individuals in activities of daily life, its recognition emphasizes the need to review measures to prevent accidental transmissions via other medical and surgical procedures. As propagating Aβ assemblies may exhibit structural diversity akin to conventional prions, it is possible that therapeutic strategies targeting disease-related assemblies may lead to selection of minor components and development of resistance.
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.