ArticleProceedings of the National Academy of Sciences of the United States of America2017
Evidence for sortilin modulating regional accumulation of human tau prions in transgenic mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. 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, 27 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Differentially expressed miRNAs in the temporal cortex of Alzheimer's disease patients and their association to tau pathology.Communications biology · 2026Article
- Microbial Composition, Disease Trajectory and Genetic Background in a Slow Onset Model of Frontotemporal Lobar Degeneration.Biomolecules · 2025Article
- Interacting MeZFP29 and MebZIPW regulates MeNRT2.2 from cassava responding to nitrate signaling.Plant cell reports · 2025Article
- Animal models of Alzheimer's disease: Current strategies and new directions.Zoological research · 2024Review
- Severe neurodegeneration in brains of transgenic rats producing human tau prions.Acta neuropathologica · 2024Article
- Glymphatic inhibition exacerbates tau propagation in an Alzheimer's disease model.Alzheimer's research & therapy · 2024Article
- MSUT2 regulates tau spreading via adenosinergic signaling mediated ASAP1 pathway in neurons.Acta neuropathologica · 2024Article
- Neuronal tau pathology worsens late-phase white matter degeneration after traumatic brain injury in transgenic mice.Acta neuropathologica · 2023Article
- Guam ALS-PDC is a distinct double-prion disorder featuring both tau and Aβ prions.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Early Post-ischemic Brain Glucose Metabolism Is Dependent on Function of TLR2: a Study Using [Molecular imaging and biology · 2022Article
- Hampering the early aggregation of PrP-E200K protein by charge-based inhibitors: a computational study.Journal of computer-aided molecular design · 2021Article
- Tau aggregates are RNA-protein assemblies that mislocalize multiple nuclear speckle components.Neuron · 2021Article
- Aβ and tau prion-like activities decline with longevity in the Alzheimer's disease human brain.Science translational medicine · 2019Article
- Regional and Cellular Mapping of Sortilin Immunoreactivity in Adult Human Brain.Frontiers in neuroanatomy · 2019Article
- Intercellular Spread of Protein Aggregates in Neurodegenerative Disease.Annual review of cell and developmental biology · 2018Review
- Selective vulnerability in neurodegenerative diseases.Nature neuroscience · 2018Review
- Lack of human-like extracellular sortilin neuropathology in transgenic Alzheimer's disease model mice and macaques.Alzheimer's research & therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Misfolding of tau proteins into prions and their propagation along neural circuits are thought to result in neurodegeneration causing Alzheimer's disease, progressive supranuclear palsy, chronic traumatic encephalopathy, and other tauopathies. Little is known about the molecular processes mediating tau prion replication and spreading in different brain regions. Using transgenic (Tg) mice with a neuronal promoter driving expression of human mutant (P301S) tau, we found that tau prion formation and histopathologic deposition is largely restricted to the hindbrain. Unexpectedly, tau mRNA and protein levels did not differ between the forebrain and hindbrain, suggesting that other factors modulating the conversion of tau into a prion exist and are region specific. Using a cell-based prion propagation assay, we discovered that tau prion replication is suppressed by forebrain-derived inhibitors, one of which is sortilin, a lysosomal sorting receptor. We also show that sortilin expression is higher in the forebrain than the hindbrain across the life span of the Tg mice, suggesting that sortilin, at least in part, inhibits forebrain tau prion replication in vivo. Our findings provide evidence for selective vulnerability in mice resulting in highly regulated levels of tau prion propagation, thus affording a model for identification of additional molecules that could mitigate the levels of tau prions in human tauopathies.
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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.