ArticleActa neuropathologica communications2018
Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression.
Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- De novo formation of familial Alzheimer's disease-relevant Aβ strains occurs exclusively in the human brain.Acta neuropathologica communications · 2026Article
- Prion-like transmission and propagation of human β-amyloid to the bank vole rodent model.Acta neuropathologica · 2026Article
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
- [18F]flutemetamol uptake in the colon of a memory clinic population and its association with brain amyloidosis and the gut microbiota profile: an exploratory study.European journal of nuclear medicine and molecular imaging · 2025Article
- Experimental evidence that readily diffusible forms of Aβ from Alzheimer's disease brain have seeding activity.Acta neuropathologica communications · 2025Article
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- Trajectory of brain-derived amyloid beta in Alzheimer's disease: where is it coming from and where is it going?Translational neurodegeneration · 2024Review
- Astemizole, a Second-Generation Histamine H1-Receptor Antagonist, Did Not Attenuate the Aggregation Process of α-Synuclein In Vitro.Biomedicines · 2024Article
- Emergence of the brain-border immune niches and their contribution to the development of neurodegenerative diseases.Frontiers in immunology · 2024Review
- Mechanisms of Intracellular Communication in Cancer and Pathogen Spreading.Results and problems in cell differentiation · 2024Review
- "Prion-like" seeding and propagation of oligomeric protein assemblies in neurodegenerative disorders.Frontiers in neuroscience · 2024Review
- Opinion: more mouse models and more translation needed for ALS.Molecular neurodegeneration · 2023Review
- Review
- The Pathological Effects of Circulating Hydrophobic Bile Acids in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Review
- Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The course of primary progressive aphasia diagnosis: a cross-sectional study.Alzheimer's research & therapy · 2022Article
- The mTOR-lysosome axis at the centre of ageing.FEBS open bio · 2022Review
- Effects of oligomer toxicity, fibril toxicity and fibril spreading in synucleinopathies.Cellular and molecular life sciences : CMLS · 2022Review
- Deciphering the Structure and Formation of Amyloids in Neurodegenerative Diseases With Chemical Biology Tools.Frontiers in chemistry · 2022Review
- The effect of Aβ seeding is dependent on the presence of knock-in genes in theFrontiers in dementia · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The amyloid cascade hypothesis posits that the initiating event in Alzheimer's disease (AD) is the aggregation and deposition of the β-amyloid (Aβ) peptide, which is a proteolytic cleavage product of the amyloid precursor protein (APP). Mounting evidence suggests that the formation and spread of prion-like Aβ aggregates during AD may contribute to disease progression. Inoculation of transgenic mice that overexpress APP with pre-formed Aβ aggregates results in the prion-like induction of cerebral Aβ deposition. To determine whether Aβ deposition can also be induced when physiological APP levels are present in the brain, we inoculated App
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