ArticleThe Journal of biological chemistry2015
Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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
77 citing papers in PubMed, 129 citations in OpenAlex.
- 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
- Therapeutic potential of mesenchymal stem cells in neurodegenerative diseases.World journal of stem cells · 2025Review
- The Potential Regulators of Amyloidogenic Pathway of APP Processing in Alzheimer's Disease.Biomedicines · 2025Review
- Acute targeting of N-terminal tau protein has long-lasting beneficial effects in Tg2576 APP/Aβ mouse model by reducing cognitive impairment, cerebral Aβ-amyloidosis, synaptic remodeling and microgliosis later in life.Acta neuropathologica communications · 2025Article
- Serotonergic Regulation in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?International journal of molecular sciences · 2025Review
- α-Synuclein strain propagation is independent of cellular prion protein expression in a transgenic synucleinopathy mouse model.PLoS pathogens · 2024Article
- Solid-state NMR studies of proteins in condensed phases.Magnetic resonance letters · 2024Review
- Structural Variations of Prions and Prion-like Proteins Associated with Neurodegeneration.Current issues in molecular biology · 2024Review
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- Neuronal transcriptome, tau and synapse loss in Alzheimer's knock-in mice require prion protein.Alzheimer's research & therapy · 2023Article
- Inducing prion protein shedding as a neuroprotective and regenerative approach in pathological conditions of the brain: from theory to facts.Neural regeneration research · 2023Review
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- Review
- 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
- Imbalance of Essential Metals in Traumatic Brain Injury and Its Possible Link with Disorders of Consciousness.International journal of molecular sciences · 2023Review
- Chemiexcitation: Mammalian Photochemistry in the DarkPhotochemistry and photobiology · 2023Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer disease (AD) is characterized by amyloid-β accumulation, with soluble oligomers (Aβo) being the most synaptotoxic. However, the multivalent and unstable nature of Aβo limits molecular characterization and hinders research reproducibility. Here, we characterized multiple Aβo forms throughout the life span of various AD mice and in post-mortem human brain. Aβo exists in several populations, where prion protein (PrP(C))-interacting Aβo is a high molecular weight Aβ assembly present in multiple mice and humans with AD. Levels of PrP(C)-interacting Aβo match closely with mouse memory and are equal or superior to other Aβ measures in predicting behavioral impairment. However, Aβo metrics vary considerably between mouse strains. Deleting PrP(C) expression in mice with relatively low PrP(C)-interacting Aβo (Tg2576) results in partial rescue of cognitive performance as opposed to complete recovery in animals with a high percentage of PrP(C)-interacting Aβo (APP/PSEN1). These findings highlight the relative contributions and interplay of Aβo forms in AD.
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.