ArticleActa neuropathologica communications2021
Amyloid pathology arrangements in Alzheimer's disease brains modulate in vivo seeding capability.
Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 28 citations in OpenAlex.
- Brain-seeded 42-residue Amyloid-β Fibrils That Resemble Fibrils Directly Extracted From Alzheimer's Disease Brain Tissue.Journal of molecular biology · 2026Article
- De novo formation of familial Alzheimer's disease-relevant Aβ strains occurs exclusively in the human brain.Acta neuropathologica communications · 2026Article
- Ex vivo comparison of ACU193 and lecanemab reveals binding differences in mouse brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.Brain communications · 2026Article
- Article
- Human and Mouse Alzheimer's Seeds Differentially Affect Amyloid Deposition and Microglia-Dependent Plaque Response in Aged Mice.Aging cell · 2025Article
- Unveiling the Interplay: Neurovascular Coupling, Astrocytes and G Protein-Coupled Receptors in Alzheimer's Disease.ACS pharmacology & translational science · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- In silico analysis of the use of solanine derivatives as a treatment for Alzheimer's disease.Heliyon · 2024Article
- The Single Toxin Origin of Alzheimer's Disease and Other Neurodegenerative Disorders Enables Targeted Approach to Treatment and Prevention.International journal of molecular sciences · 2024Review
- Linderae Radix Ameliorates Cognitive Dysfunction by Inhibiting Neuroinflammation and Synaptic Damage in Alzheimer's Disease Models.Molecular neurobiology · 2023Article
- Two structurally defined Aβ polymorphs promote different pathological changes in susceptible mice.EMBO reports · 2023Article
- Misfolded amyloid-β strains and their potential roles in the clinical and pathological variability of Alzheimer's disease.Neural regeneration research · 2023Article
- Synthetic, Cell-Derived, Brain-Derived, and Recombinant β-Amyloid: Modelling Alzheimer's Disease for Research and Drug Development.International journal of molecular sciences · 2022Review
- Transmission of Cerebral β-Amyloidosis Among Individuals.Neurochemical research · 2022Article
- Multi-Dose Intravenous Administration of Neutral and Cationic Liposomes in Mice: An Extensive Toxicity Study.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis.International journal of molecular sciences · 2022Review
- The clock modulator Nobiletin mitigates astrogliosis-associated neuroinflammation and disease hallmarks in an Alzheimer's disease model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Recent update on the heterogeneity of the Alzheimer's disease spectrum.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Expanding the family of extracellular chaperones: Identification of human plasma proteins with chaperone activity.Protein science : a publication of the Protein Society · 2021Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Amyloid-β (Aβ) misfolding is one of the hallmark pathological features of Alzheimer's disease (AD). AD can manifest with diverse symptomatology including variable rates of cognitive decline, duration of clinical disease, and other detrimental changes. Several reports suggest that conformational diversity in misfolded Aβ is a leading factor for clinical variability in AD, analogous to what it has been described for prion strains in prion diseases. Notably, prion strains generate diverse patterns of misfolded protein deposition in the brains of affected individuals. Here, we tested the in vivo prion-like transmission features of four AD brains displaying particular patterns of amyloidosis. AD brains induced different phenotypes in recipient mice, as evaluated by their specific seeding activity, as well as the total amount of Aβ deposited surrounding vascular structures and the reactivity of amyloid pathology to thioflavin S. Our results support the notion that AD-subtypes are encoded in disease-associated Aβ. Further research exploring whether AD include a spectrum of different clinical conditions or syndromes may pave the way to personalized diagnosis and treatments.
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Registered trials
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