ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020
Administration of FK506 from Late Stage of Disease Prolongs Survival of Human Prion-Inoculated Mice.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Sporadic Creutzfeldt-Jakob disease: a multidimensional review from epidemiology to treatment and prognosis.Journal of neurology · 2026Review
- One organelle to rule them all: enhancement of lysosomal activity as a therapeutic modality for protein misfolding neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- Knockout of P2Y12 receptor facilitates neuronal envelopment by reactive microglia and accelerates prion disease.Journal of neuroinflammation · 2025Article
- Knockout of P2Y12 receptor facilitates microglia-neuron body-to-body interactions and accelerates prion disease.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of the Factors Influencing the Survival Times of Chinese Patients with Probable Creutzfeldt-Jacob Disease - China, 2020-2022.China CDC weekly · 2025Article
- Article
- New Therapeutic Modalities in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Article
- Altered DNA methylation profiles in blood from patients with sporadic Creutzfeldt-Jakob disease.Acta neuropathologica · 2020Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human prion diseases are etiologically categorized into three forms: sporadic, genetic, and infectious. Sporadic Creutzfeldt-Jakob disease (sCJD) is the most common type of human prion disease that manifests as subacute progressive dementia. No effective therapy for sCJD is currently available. Potential therapeutic compounds are frequently tested in rodents infected with mouse-adapted prions that differ from human prions. However, therapeutic effect varies depending on the prion strain, which is one of the reasons why candidate compounds have shown little effect in sCJD patients. We previously reported that intraperitoneal administration of FK506 was able to prolong the survival of mice infected with a mouse-adapted prion by suppressing the accumulation of abnormal prion protein (PrP) and inhibiting the activation of microglia. In this study, we tested oral administration of FK506 in knock-in mice expressing chimeric human prion protein (KiChM) that were infected with sCJD to determine if this compound is also effective against a clinically relevant human prion, i.e., one that has not been adapted to mice. Treatment with FK506, started either just before or just after disease onset, suppressed typical sCJD pathology (gliosis) and slightly but significantly prolonged the survival of sCJD-inoculated mice. It would be worthwhile to conduct a clinical trial using FK506, which has been safety-approved and is widely used as a mild immunosuppressant.
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