ReviewInternational journal of molecular sciences2025
Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Synthesis of Phenyl 2-Acetamidoselenogalactoside Mimetics and Interaction with Amyloid βPharmaceuticals (Basel, Switzerland) · 2026Article
- Small-Molecule Targeting of the Iron-Responsive Element in the APP mRNA 5'-UTR to Control Amyloid Translation in Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Beyond the neuron: Exosomes as intercellular modulators of mitochondrial networks in the pathogenesis and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Perspectives on Alzheimer's Disease Treatment Based on Counteracting Oxidative Stress.Biomolecules · 2025Review
- The Potential Regulators of Amyloidogenic Pathway of APP Processing in Alzheimer's Disease.Biomedicines · 2025Review
- Iron-Mediated Overexpression of Amyloid Precursor Protein via Iron Responsive mRNA in Alzheimer's Disease.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia worldwide. Pathological deposits of neurotoxin proteins within the brain, such as amyloid-β and hyperphosphorylated tau tangles, are prominent features in AD. The prion protein (PrP) is involved in neurodegeneration via its conversion from the normal cellular form (PrPC) to the infection prion protein scrapie (PrPSc) form. Some studies indicated that post-translationally modified PrPC isoforms play a fundamental role in AD pathological progression. Several studies have shown that the interaction of Aβ oligomers (Aβos) with the N-terminal residues of the PrPC protein region appears critical for neuronal toxicity. PrPC-Aβ binding always occurs in AD brains and is never detected in non-demented controls, and the binding of Aβ aggregates to PrPC is restricted to the N-terminus of PrPC. In this study, we aimed to gather all of the recent information about the connections between PrPC and AD, with potential clinical implications.
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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 Socratic graph.