ArticleMolecular psychiatry2018
Blood-derived amyloid-β protein induces Alzheimer's disease pathologies.
Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 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
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Who cites it
129 citing papers in PubMed, 231 citations in OpenAlex.
- Association Between Plasma Amyloid-Beta 42 Ratio and Postoperative Delirium in Elderly Patients Undergoing Major Abdominal Surgery: Secondary Analysis of a Randomized Controlled Trial.Brain and behavior · 2025Trial
- Effects of Probucol on plasma amyloid-β transport in patients with hyperlipidemia: a 12-week randomized, double-blind, placebo-controlled trial.Lipids in health and disease · 2024Trial
- β-Amyloid accumulation in the human brain after one night of sleep deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2018Trial
- Transcriptional risk score for chronic kidney disease: relation to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Body-Wide Glycolytic Shift, Oxidative Stress, and Sex-Specific Effect of Caloric Restriction in a Mouse Model of Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- The diagnostic value of plasma Aβ42 and Aβ40 in Alzheimer's disease: current status, challenges, and impacting variables.Journal of neurology · 2025Review
- The relationship between choroid plexus volume, DTI-ALPS index, kidney function, and amyloid pathology in alzheimer's disease.Neuroradiology · 2025Article
- Parkinson's Disease: The Epidemiology, Risk Factors, Molecular Pathogenesis, Prevention, and Therapy.MedComm · 2025Review
- Proteomic signatures and mitochondrial dysfunctions in peripheral T cells reveal novel ınsights into Alzheimer's disease.Scientific reports · 2025Article
- SIK2-mediated phosphorylation of GABARAPL2 facilitates autophagosome-lysosome fusion and rescues neurodegeneration in an Alzheimer's disease model.Translational neurodegeneration · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- APOE4 Exacerbates Alzheimer-Like Pathologies and Cognitive Deficits Induced by Blood-Derived Aβ in a Mouse Model.Aging cell · 2025Article
- Endothelial delivery of simvastatin by LRP1-targeted nanoparticles ameliorates pathogenesis of alzheimer's disease in a mouse model.Alzheimer's research & therapy · 2025Article
- The effect of NF-kB and MAPK mediated Proinflammatory microenvironment on renal aging and amyloid deposition in elder rats.Scientific reports · 2025Article
- Human and Mouse Alzheimer's Seeds Differentially Affect Amyloid Deposition and Microglia-Dependent Plaque Response in Aged Mice.Aging cell · 2025Article
- Ultrasonic disruption of circulating amyloid β aggregates via phase-change peptide nanoemulsions.Biomaterials · 2025Article
- Could Blood Transfusion Increase the Risk of Alzheimer's Disease? A Narrative Review.Healthcare (Basel, Switzerland) · 2025Review
- Peripheral administration of blood from tau transgenic animals exacerbates brain tau-associated pathology.PloS one · 2025Article
- A Novel Perspective on PCSK9 in Alzheimer's Disease: A Focus on Amyloid Beta.Current medicinal chemistry · 2025Review
69 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 9 institutions in 4 countries.
Funding
Abstract
The amyloid-β protein (Aβ) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aβ deposited in the brain originates from the brain tissue itself. However, Aβ is generated in both brain and peripheral tissues. Whether circulating Aβ contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aβ originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aβ plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aβ accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aβ can enter the brain, form the Aβ-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aβ metabolism in both the brain and the periphery.
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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 Socratic graph.