ReviewIntractable & rare diseases research2013
Alzheimer's disease and prion protein.
Review in Intractable & rare diseases research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 29 citations in OpenAlex.
- Exploring the Biological Connection Between Tau and PrPMolecular neurobiology · 2025Review
- Novel anti-prion compounds screening in prion-infected cell culture model combined with surface plasmon resonance analysis.Scientific reports · 2025Article
- Cognitive improvement effects of PF-04957325, a phosphodiesterase-8 inhibitor, in mouse models of Alzheimer's disease via modulating neuroinflammation.The international journal of neuropsychopharmacology · 2025Article
- Comprehensive investigation of multiple targets in the development of newer drugs for the Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Review
- Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?International journal of molecular sciences · 2025Review
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- Review
- Article
- Infections and immunity: associations with obesity and related metabolic disorders.Journal of pathology and translational medicine · 2023Review
- Astrocytic MicroRNAs and Transcription Factors in Alzheimer's Disease and Therapeutic Interventions.Cells · 2022Review
- Affinity Purification of Glycosylphosphatidylinositol-anchored Proteins by Alpha-Toxin.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Effects of fibrinogen synthesis inhibition on vascular cognitive impairment during traumatic brain injury in mice.Brain research · 2021Article
- Fibrinogen-cellular prion protein complex formation on astrocytes.Journal of neurophysiology · 2020Article
- Nanotechnology to improve the Alzheimer's disease therapy with natural compounds.Drug delivery and translational research · 2020Review
- Down syndrome: A curative prospect?AIMS neuroscience · 2020Review
- Vascular and non-vascular contributors to memory reduction during traumatic brain injury.The European journal of neuroscience · 2019Review
- The mammalian CTLH complex is an E3 ubiquitin ligase that targets its subunit muskelin for degradation.Scientific reports · 2019Article
- Design and Synthesis of CNS-targeted Flavones and Analogues with Neuroprotective Potential Against HPharmaceuticals (Basel, Switzerland) · 2019Article
- Effects of Prion Protein on Aβ42 and Pyroglutamate-Modified AβpΕ3-42 Oligomerization and Toxicity.Molecular neurobiology · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a devastating neurodegenerative disease with progressive loss of memory and cognitive function, pathologically hallmarked by aggregates of the amyloid-beta (Aβ) peptide and hyperphosphorylated tau in the brain. Aggregation of Aβ under the form of amyloid fibrils has long been considered central to the pathogenesis of AD. However, recent evidence has indicated that soluble Aβ oligomers, rather than insoluble fibrils, are the main neurotoxic species in AD. The cellular prion protein (PrP(C)) has newly been identified as a cell surface receptor for Aβ oligomers. PrP(C) is a cell surface glycoprotein that plays a key role in the propagation of prions, proteinaceous infectious agents that replicate by imposing their abnormal conformation to PrP(C) molecules. In AD, PrP(C) acts to transduce the neurotoxic signals arising from Aβ oligomers, leading to synaptic failure and cognitive impairment. Interestingly, accumulating evidence has also shown that aggregated Aβ or tau possesses prion-like activity, a property that would allow them to spread throughout the brain. In this article, we review recent findings regarding the function of PrP(C) and its role in AD, and discuss potential therapeutic implications of PrP(C)-based approaches in the treatment of AD.
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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.