ReviewNeural regeneration research2018
Targeting prion-like protein spreading in neurodegenerative diseases.
Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 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.
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
14 citing papers in PubMed, 38 citations in OpenAlex.
- Amyloid-β, Tau Protein, α-Synuclein, TDP-43, and FUS in Mixed Pathology: And Intrinsic Disorder to Rule Them All.International journal of molecular sciences · 2026Review
- Catalytic Proximal Protein Oligomerization as an Anti-Tumor Strategy Targeting WDR5.Nature communications · 2026Article
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- Semantic dementia: a complex and culturally influenced presentation.BJPsych bulletin · 2024Article
- Enhanced growth and differentiation of neural stem cells on alginate/collagen/reduced graphene oxide composite hydrogel incorporated with lithium chloride.BioImpacts : BI · 2023Article
- Article
- Elucidating the Multi-Targeted Role of Nutraceuticals: A Complementary Therapy to Starve Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Pharmacological Inhibition of Brain EGFR Activation By a BBB-penetrating Inhibitor, AZD3759, Attenuates α-synuclein Pathology in a Mouse Model of α-Synuclein Propagation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Peripherally misfolded proteins exacerbate ischemic stroke-induced neuroinflammation and brain injury.Journal of neuroinflammation · 2021Article
- Testing Amyloid Cross-Toxicity in the Vertebrate Brain.ACS omega · 2020Article
- Neuroprotective Effect of Brazilin on Amyloid β (25-35)-Induced Pathology in a Human Neuroblastoma Model.ACS omega · 2020Article
- Review
- The road ahead in clinical network neuroscience.Network neuroscience (Cambridge, Mass.) · 2019Review
- Corrigendum: Targeting prion-like protein spreading in neurodegenerative diseases.Neural regeneration research · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The infectious template-mediated protein conversion is a unique mechanism for the onset of rare and fatal neurodegenerative disorders known as transmissible spongiform encephalopathies, or prion diseases, which affect humans and other animal species. However, emerging studies are now demonstrating prion-like mechanisms of self-propagation of protein misfolding in a number of common, non-infectious neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. It has been proposed that distinct and unrelated proteins (beta-amyloid, tau, α-synuclein, TAR DNA-binding protein 43 and huntingtin, etc.) associated with common neurodegenerative disorders can seed conversion and spread via cell-to-cell transfer, sustaining the transmission of neurotoxic agents along a stereotypic route, sharing features at the heart of the intrinsic nature of prions. Here we review the most recent development on both the molecular mechanisms underlying the pathogenesis of prion-like neurodegenerative diseases as well as innovative methods and strategies for potential therapeutic applications.
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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.