ArticlePLoS biology2016
Distribution of Misfolded Prion Protein Seeding Activity Alone Does Not Predict Regions of Neurodegeneration.
Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Presymptomatic pharmacological inhibition of mGluR5 improves survival in a mouse model of prion diseases.Acta neuropathologica communications · 2026Article
- Overview of Metformin and Neurodegeneration: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The dynamics of prion spreading is governed by the interplay between the non-linearities of tissue response and replication kinetics.iScience · 2024Article
- Innate Immune Tolerance in Microglia Does Not Impact on Central Nervous System Prion Disease.Frontiers in cellular neuroscience · 2022Article
- Linking Stage-Specific Plasma Biomarkers to Gray Matter Atrophy in Parkinson Disease.AJNR. American journal of neuroradiology · 2021Article
- Novel Morphological Glial Alterations in the Spectrum of Prion Disease Types: A Focus on Common Findings.Pathogens (Basel, Switzerland) · 2021Article
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Quaternary Structure Changes for PrPMolecular neurobiology · 2021Article
- Regional Differences in Neuroinflammation-Associated Gene Expression in the Brain of Sporadic Creutzfeldt-Jakob Disease Patients.International journal of molecular sciences · 2020Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Defining the Protein Seeds of Neurodegeneration using Real-Time Quaking-Induced Conversion Assays.Biomolecules · 2020Review
- Pathogenic Prion Protein Isoforms Are Not Present in Cerebral Organoids Generated from Asymptomatic Donors Carrying the E200K Mutation Associated with Familial Prion Disease.Pathogens (Basel, Switzerland) · 2020Article
- Assessment of Glial Activation Response in the Progress of Natural Scrapie after Chronic Dexamethasone Treatment.International journal of molecular sciences · 2020Article
- Cellulose ether treatment in vivo generates chronic wasting disease prions with reduced protease resistance and delayed disease progression.Journal of neurochemistry · 2020Article
- Intrastriatal Administration of Exosome-Associated Pathological Alpha-Synuclein Is Not Sufficient by Itself to Cause Pathology Transmission.Frontiers in neuroscience · 2020Article
- Tau Misfolding Efficiently Propagates between Individual Intact Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Review
- TREM2 - a key player in microglial biology and Alzheimer disease.Nature reviews. Neurology · 2018Review
- Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?Prion · 2018Article
- What is the evidence that tau pathology spreads through prion-like propagation?Acta neuropathologica communications · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Protein misfolding is common across many neurodegenerative diseases, with misfolded proteins acting as seeds for "prion-like" conversion of normally folded protein to abnormal conformations. A central hypothesis is that misfolded protein accumulation, spread, and distribution are restricted to specific neuronal populations of the central nervous system and thus predict regions of neurodegeneration. We examined this hypothesis using a highly sensitive assay system for detection of misfolded protein seeds in a murine model of prion disease. Misfolded prion protein (PrP) seeds were observed widespread throughout the brain, accumulating in all brain regions examined irrespective of neurodegeneration. Importantly, neither time of exposure nor amount of misfolded protein seeds present determined regions of neurodegeneration. We further demonstrate two distinct microglia responses in prion-infected brains: a novel homeostatic response in all regions and an innate immune response restricted to sites of neurodegeneration. Therefore, accumulation of misfolded prion protein alone does not define targeting of neurodegeneration, which instead results only when misfolded prion protein accompanies a specific innate immune response.
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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.