ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Conditional Deletion of
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Distinct Filament Conformation for Receptor-Bound Amyloid-β from Alzheimer's Disease Brain.Nature communications · 2026Article
- Genome-wide screens identify core regulators of cell surface prion protein expression.Scientific reports · 2026Article
- Distinct Filament Conformation for Receptor-Bound Amyloid-ß from Alzheimer's Disease Brain.bioRxiv : the preprint server for biology · 2025Article
- Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice.The Journal of clinical investigation · 2025Article
- Loss of the APP regulator RHBDL4 preserves memory in an Alzheimer's disease mouse model.Cell death & disease · 2025Article
- Neuronal transcriptome, tau and synapse loss in Alzheimer's knock-in mice require prion protein.Alzheimer's research & therapy · 2023Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- Sigma-2 Receptors-From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases.International journal of molecular sciences · 2023Review
- primiReference: a reference for analysis of primary-microRNA expression in single-nucleus sequencing data.Journal of genetics and genomics = Yi chuan xue bao · 2023Article
- Review
- The multiple functions of PrPJournal of molecular medicine (Berlin, Germany) · 2022Review
- Reversal of synapse loss in Alzheimer mouse models by targeting mGluR5 to prevent synaptic tagging by C1Q.Science translational medicine · 2022Article
- Analysis of co-isogenic prion protein deficient mice reveals behavioral deficits, learning impairment, and enhanced hippocampal excitability.BMC biology · 2022Article
- The probabilistic model of Alzheimer disease: the amyloid hypothesis revised.Nature reviews. Neuroscience · 2022Review
- Discovering new peripheral plasma biomarkers to identify cognitive decline in type 2 diabetes.Frontiers in cell and developmental biology · 2022Article
- Accumulation of cellular prion protein within β-amyloid oligomer plaques in aged human brains.Brain pathology (Zurich, Switzerland) · 2021Article
- Aβ receptors specifically recognize molecular features displayed by fibril ends and neurotoxic oligomers.Nature communications · 2021Article
- Structural Features and Toxicity of α-Synuclein Oligomers Grown in the Presence of DOPAC.International journal of molecular sciences · 2021Article
- Amyloid binding and beyond: a new approach for Alzheimer's disease drug discovery targeting Aβo-PrPChemical science · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Biochemical and genetic evidence implicate soluble oligomeric amyloid-β (Aβo) in triggering Alzheimer's disease (AD) pathophysiology. Moreover, constitutive deletion of the Aβo-binding 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.