ArticleJournal of neurochemistry2012
Exogenous seeding of cerebral β-amyloid deposition in βAPP-transgenic rats.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 119 citations in OpenAlex.
- Prion-like transmission and propagation of human β-amyloid to the bank vole rodent model.Acta neuropathologica · 2026Article
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- Review
- Switching On/Off Amyloid Plaque Formation in Transgenic Animal Models of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Transmission of Cerebral β-Amyloidosis Among Individuals.Neurochemical research · 2022Article
- Support vector machine learning and diffusion-derived structural networks predict amyloid quantity and cognition in adults with Down's syndrome.Neurobiology of aging · 2022Article
- A History of Senile Plaques: From Alzheimer to Amyloid Imaging.Journal of neuropathology and experimental neurology · 2022Article
- Association Plasma Aβ42 Levels with Alzheimer's Disease and Its Influencing Factors in Chinese Elderly Population.Neuropsychiatric disease and treatment · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Neuronal spreading and plaque induction of intracellular Aβ and its disruption of Aβ homeostasis.Acta neuropathologica · 2021Article
- Precocious White Matter Inflammation and Behavioural Inflexibility Precede Learning and Memory Impairment in the TgAPP21 Rat Model of Alzheimer Disease.Molecular neurobiology · 2021Article
- MicroRNAs in Prion Diseases-From Molecular Mechanisms to Insights in Translational Medicine.Cells · 2021Review
- Atomic-level differences between brain parenchymal- and cerebrovascular-seeded Aβ fibrils.Scientific reports · 2021Article
- Aged Cattle Brain Displays Alzheimer's Disease-Like Pathology and Promotes Brain Amyloidosis in a Transgenic Animal Model.Frontiers in aging neuroscience · 2021Article
- White matter inflammation and cognitive function in a co-morbid metabolic syndrome and prodromal Alzheimer's disease rat model.Journal of neuroinflammation · 2020Article
- Hypertension and Pathogenic hAPP Independently Induce White Matter Astrocytosis and Cognitive Impairment in the Rat.Frontiers in aging neuroscience · 2020Article
- Prion and Prion-Like Protein Strains: Deciphering the Molecular Basis of Heterogeneity in Neurodegeneration.Viruses · 2019Review
- Aβ Seeding as a Tool to Study Cerebral Amyloidosis and Associated Pathology.Frontiers in molecular neuroscience · 2019Review
- Tau covariance patterns in Alzheimer's disease patients match intrinsic connectivity networks in the healthy brain.NeuroImage. Clinical · 2019Article
- Intercellular Spread of Protein Aggregates in Neurodegenerative Disease.Annual review of cell and developmental biology · 2018Review
9 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Deposition of the amyloid-β (Aβ) peptide in senile plaques and cerebral Aβ angiopathy (CAA) can be stimulated in Aβ-precursor protein (APP)-transgenic mice by the intracerebral injection of dilute brain extracts containing aggregated Aβ seeds. Growing evidence implicates a prion-like mechanism of corruptive protein templating in this phenomenon, in which aggregated Aβ itself is the seed. Unlike prion disease, which can be induced de novo in animals that are unlikely to spontaneously develop the disease, previous experiments with Aβ seeding have employed animal models that, as they age, eventually will generate Aβ lesions in the absence of seeding. In the present study, we first established that a transgenic rat model expressing human APP (APP21 line) does not manifest endogenous deposits of Aβ within the course of its median lifespan (30 months). Next, we injected 3-month-old APP21 rats intrahippocampally with dilute Alzheimer brain extracts containing aggregated Aβ. After a 9-month incubation period, these rats had developed senile plaques and CAA in the injected hippocampus, whereas control rats remained free of such lesions. These findings underscore the co-dependence of agent and host in governing seeded protein aggregation, and show that cerebral Aβ-amyloidosis can be induced even in animals that are relatively refractory to the spontaneous origination of parenchymal and vascular deposits of Aβ.
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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.