ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Multiple factors contribute to the peripheral induction of cerebral β-amyloidosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 87 citations in OpenAlex.
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
- Article
- Sex-specific effects of chronic alcohol consumption across the lifespan in the transgenic Alzheimer's Disease (TgF344-AD) rat model.Brain, behavior, and immunity · 2025Article
- In Vivo Seeding of Amyloid-β Protein and Implications in Modeling Alzheimer's Disease Pathology.Biomolecules · 2025Review
- Cellular Prion Protein and Amyloid-β Oligomers in Alzheimer's Disease-Are There Connections?International journal of molecular sciences · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Iatrogenic Alzheimer's disease in recipients of cadaveric pituitary-derived growth hormone.Nature medicine · 2024Article
- Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease.Aging and disease · 2024Review
- Post-translational modifications of beta-amyloid alter its transport in the blood-brain barrierFrontiers in molecular neuroscience · 2024Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- Article
- Transmission of Cerebral β-Amyloidosis Among Individuals.Neurochemical research · 2022Article
- Isotope-labeled amyloid-β does not transmit to the brain in a prion-like manner after peripheral administration.EMBO reports · 2022Article
- Soluble brain homogenates from diverse human and mouse sources preferentially seed diffuse Aβ plaque pathology when injected into newborn mouse hosts.Free neuropathology · 2022Article
- The Blood-Brain Barrier in Alzheimer's Disease.Handbook of experimental pharmacology · 2022Article
- The Role of Circulating Aβ Seeds in the Progression of Cerebral Amyloidosis.Neuroscience insights · 2022Article
- Blood cell-produced amyloid-β induces cerebral Alzheimer-type pathologies and behavioral deficits.Molecular psychiatry · 2021Article
- Amyloid pathology arrangements in Alzheimer's disease brains modulate in vivo seeding capability.Acta neuropathologica communications · 2021Article
- Remodeling Alzheimer-amyloidosis models by seeding.Molecular neurodegeneration · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deposition of aggregated amyloid-β (Aβ) peptide in brain is an early event and hallmark pathology of Alzheimer's disease and cerebral Aβ angiopathy. Experimental evidence supports the concept that Aβ multimers can act as seeds and structurally corrupt other Aβ peptides by a self-propagating mechanism. Here we compare the induction of cerebral β-amyloidosis by intraperitoneal applications of Aβ-containing brain extracts in three Aβ-precursor protein (APP) transgenic mouse lines that differ in levels of transgene expression in brain and periphery (APP23 mice, APP23 mice lacking murine APP, and R1.40 mice). Results revealed that beta-amyloidosis induction, which could be blocked with an anti-Aβ antibody, was dependent on the amount of inoculated brain extract and on the level of APP/Aβ expression in the brain but not in the periphery. The induced Aβ deposits in brain occurred in a characteristic pattern consistent with the entry of Aβ seeds at multiple brain locations. Intraperitoneally injected Aβ could be detected in blood monocytes and some peripheral tissues (liver, spleen) up to 30 d after the injection but escaped histological and biochemical detection thereafter. These results suggest that intraperitoneally inoculated Aβ seeds are transported from the periphery to the brain in which corruptive templating of host Aβ occurs at multiple sites, most efficiently in regions with high availability of soluble Aβ.
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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.