ReviewFrontiers in cellular neuroscience2019
Cellular Prion Protein as a Receptor of Toxic Amyloid-β42 Oligomers Is Important for Alzheimer's Disease.
Review in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- CT1812 biomarker signature from a meta-analysis of CSF proteomic findings from two Phase 2 clinical trials in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Pooled it
- Prion-like transmission and propagation of human β-amyloid to the bank vole rodent model.Acta neuropathologica · 2026Article
- Oral Microbiome-Derived Proteins in Brain Extracellular Vesicles Circulate and Tie to Specific Dysbiotic and Neuropathological Profiles in Age-Related Dementias.Molecular & cellular proteomics : MCP · 2025Article
- Lack of cellular prion protein causes Amyloid β accumulation, increased extracellular vesicle abundance, and changes to exosome biogenesis proteins.Molecular and cellular biochemistry · 2025Article
- Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?International journal of molecular sciences · 2025Review
- The cellular prion protein does not affect tau seeding and spreading of sarkosyl-insoluble fractions from Alzheimer's disease.Scientific reports · 2024Article
- Melatonin-mediated calcineurin inactivation attenuates amyloid beta-induced apoptosis.IBRO neuroscience reports · 2024Article
- Current Insights of Nanocarrier-Mediated Gene Therapeutics to Treat Potential Impairment of Amyloid Beta Protein and Tau Protein in Alzheimer's Disease.Molecular neurobiology · 2024Review
- New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024Review
- Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer's disease.Acta neuropathologica · 2024Article
- Review
- The neuroprotective N-terminal amyloid-β core hexapeptide reverses reactive gliosis and gliotoxicity in Alzheimer's disease pathology models.Journal of neuroinflammation · 2023Article
- An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer's Disease.Biomedicines · 2023Review
- Peptide aptamer targeting Aβ-PrP-Fyn axis reduces Alzheimer's disease pathologies in 5XFAD transgenic mouse model.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Review
- Comparison of Tau and Amyloid-β Targeted Immunotherapy Nanoparticles for Alzheimer's Disease.Biomolecules · 2022Review
- New Drosophila models to uncover the intrinsic and extrinsic factors that mediate the toxicity of the human prion protein.Disease models & mechanisms · 2022Article
- Brain Exosomes: Friend or Foe in Alzheimer's Disease?Molecular neurobiology · 2021Review
- Significance of Oligomeric and Fibrillar Species in Amyloidosis: Insights into Pathophysiology and Treatment.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological features of Alzheimer's disease (AD) include senile plaques induced by amyloid-β (Aβ) protein deposits, neurofibrillary tangles formed by aggregates of hyperphosphorylated tau proteins and neuronal cell loss in specific position within the brain. Recent observations have suggested the possibility of an association between AD and cellular prion protein (PrP
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.