ArticleEBioMedicine2019
Toxic amyloid-β oligomers induced self-replication in astrocytes triggering neuronal injury.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Sialic Acid-based Glycoconjugation on Myricetin-encapsulated Cationic Nanocarriers for the Treatment of Alzheimer's.Pharmaceutical research · 2025Article
- DEAD-Box Helicase 6 Blockade in Brain-Derived Aβ Oligomers From Alzheimer's Disease Patients Attenuates Neurotoxicity.MedComm · 2025Article
- Subcortical tau deposition and plasma glial fibrillary acidic protein as predictors of cognitive decline in mild cognitive impairment and Alzheimer's disease.European journal of nuclear medicine and molecular imaging · 2025Article
- Unveiling the multifaceted pathogenesis and therapeutic drugs of Alzheimer's disease: A comprehensive review.Heliyon · 2024Review
- Fluorescence-Based Monitoring of Early-Stage Aggregation of Amyloid-β, Amylin Peptide, Tau, and α-Synuclein Proteins.ACS chemical neuroscience · 2024Article
- Hybrid Amyloid Quantum Dot Nano-Bio Assemblies to Probe Neuroinflammatory Damage.ACS chemical neuroscience · 2024Article
- Roles of astrocytes and prions in Alzheimer's disease: insights from mathematical modeling.Journal of biological physics · 2024Article
- Astroglial activation: Current concepts and future directions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Sugar distributions on gangliosides guide the formation and stability of amyloid-β oligomers.Biophysical chemistry · 2023Article
- Emerging roles of astrocytes in blood-brain barrier disruption upon amyloid-beta insults in Alzheimer's disease.Neural regeneration research · 2023Review
- The interwoven fibril-like structure of amyloid-beta plaques in mouse brain tissue visualized using super-resolution STED microscopy.Cell & bioscience · 2023Article
- Genetic Phenotypes of Alzheimer's Disease: Mechanisms and Potential Therapy.Phenomics (Cham, Switzerland) · 2023Review
- A new kid in the folding funnel: Molecular chaperone activities of the BRICHOS domain.Protein science : a publication of the Protein Society · 2023Review
- Article
- The "Cerebrospinal Fluid Sink Therapeutic Strategy" in Alzheimer's Disease-From Theory to Design of Applied Systems.Biomedicines · 2022Review
- Relationship between astrocyte reactivity, using novelMolecular psychiatry · 2022Article
- The role of astrocytes in prion-like mechanisms of neurodegeneration.Brain : a journal of neurology · 2022Review
- Murine Beta-Amyloid (1-42) Oligomers Disrupt Endothelial Barrier Integrity and VEGFR Signaling via Activating Astrocytes to Release Deleterious Soluble Factors.International journal of molecular sciences · 2022Article
- The Role of Mesenchymal Stem Cells in Regulating Astrocytes-Related Synapse Dysfunction in Early Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Effects of Aβ-derived peptide fragments on fibrillogenesis of Aβ.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSoluble amyloid-β oligomer (AβO) induced deleterious cascades have recently been considered to be the initiating pathologic agents of Alzheimer's disease (AD). However, little is known about the neurotoxicity and production of different AβOs. Understanding the production and spread of toxic AβOs within the brain is important to improving understanding of AD pathogenesis and treatment.
methodsHere, PS1V97L transgenic mice, a useful tool for studying the role of AβOs in AD, were used to identify the specific AβO assembly that contributes to neuronal injury and cognitive deficits. Then, we investigated the production and spread of toxic Aβ assemblies in astrocyte and neuron cultures, and further tested the results following intracerebroventricular injection of AβOs in animal model.
findingsThe results showed that cognitive deficits were mainly caused by the accumulation of nonameric and dodecameric Aβ assemblies in the brains. In addition, we found that the toxic AβOs were duplicated in a time-dependent manner when BACE1 and apolipoprotein E were overexpressed, which were responsible for producing redundant Aβ and forming nonameric and dodecameric assemblies in astrocytes, but not in neurons.
interpretationOur results suggest that astrocytes may play a central role in the progression of AD by duplicating and spreading toxic AβOs, thus triggering neuronal injury. FUND: This study was supported by the Key Project of the National Natural Science Foundation of China; the National Key Scientific Instrument and Equipment Development Project; Beijing Scholars Program, and Beijing Brain Initiative from Beijing Municipal Science & Technology Commission.
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