ArticleCell death discovery2021
Transferrin-Pep63-liposomes accelerate the clearance of Aβ and rescue impaired synaptic plasticity in early Alzheimer's disease models.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Advances in nano-TCM for Alzheimer's disease: lipid-based carriers integrated with innovative delivery strategies.Journal of nanobiotechnology · 2026Review
- Neurexins, Ephrin receptors, and N-cadherin signaling as emerging mechanisms in synaptic dysfunction and neurodegenerative diseases.Communications biology · 2026Review
- Obesity-driven phosphatidylethanolamine dysregulation impairs neuroimmune crosstalk and accelerates Alzheimer's pathogenesis.Molecular neurodegeneration · 2026Article
- Liposomal and Nanomaterial-Based Strategies for Targeted Alzheimer's Disease Therapy.ACS omega · 2025Review
- Targeting Transferrin Receptor 1 for Enhancing Drug Delivery Through the Blood-Brain Barrier for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Atractylenolide III alleviates amyloid-β-induced cognitive impairments in mice.Molecular biology reports · 2025Article
- Utilization of nanotechnology to surmount the blood-brain barrier in disorders of the central nervous system.Materials today. Bio · 2025Review
- Drug delivery strategies with lipid-based nanoparticles for Alzheimer's disease treatment.Journal of nanobiotechnology · 2025Review
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- Nanoparticles in CNS Therapeutics: Pioneering Drug Delivery Advancements.Current pharmaceutical design · 2025Review
- Non-pharmacological treatment of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- Nanomaterials that Aid in the Diagnosis and Treatment of Alzheimer's Disease, Resolving Blood-Brain Barrier Crossing Ability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Review
- An Overview on the Physiopathology of the Blood-Brain Barrier and the Lipid-Based Nanocarriers for Central Nervous System Delivery.Pharmaceutics · 2024Review
- Long-term potentiation-based screening identifies neuronal PYGM as a synaptic plasticity regulator participating in Alzheimer's disease.Zoological research · 2023Article
- Stealth Liposomes Encapsulating a Potent ACAT1/SOAT1 Inhibitor F12511: Pharmacokinetic, Biodistribution, and Toxicity Studies in Wild-Type Mice and Efficacy Studies in Triple Transgenic Alzheimer's Disease Mice.International journal of molecular sciences · 2023Article
- Biomembrane-Derived Nanoparticles in Alzheimer's Disease Therapy: A Comprehensive Review of Synthetic Lipid Nanoparticles and Natural Cell-Derived Vesicles.International journal of nanomedicine · 2023Review
- Imaging Carotid Plaque Burden in Living Mice via Hybrid Semiconducting Polymer Nanoparticles-Based Near-Infrared-II Fluorescence and Magnetic Resonance Imaging.Research (Washington, D.C.) · 2023Article
- Transferrin-Functionalized Liposomes for the Delivery of Gallic Acid: A Therapeutic Approach for Alzheimer's Disease.Pharmaceutics · 2022Article
- Nanomedicines in the Management of Alzheimer's Disease: Current View and Future Prospects.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is characterized by aberrant accumulation of extracellular β-amyloid (Aβ) peptides in the brain. Soluble Aβ oligomers are thought to be the most neurotoxic species and are correlated with cognitive dysfunction in early AD. However, there is still no effective treatment so far. We determined that Pep63, a small peptide, had a neuroprotective effect on synaptic plasticity and memory in our previous study. Here, we developed novel and multifunctional liposomes targeting both Aβ oligomers and fibrils based on a liposome delivery system. Transferrin-Pep63-liposomes (Tf-Pep63-Lip), possessing the ability for blood-brain barrier targeting, were also incorporated with phosphatidic acid (PA) and loaded with neuroprotective Pep63. We discovered that administration of Tf-Pep63-Lip could significantly reduce the Aβ burden in the hippocampus, and improve cognitive deficits in 6-month-old APP/PS1 mice in the Morris-Water maze task and fear-conditioning test with the combined effects of PA and Pep63. Tf-Pep63-Lip could capture Aβ oligomers or fibrils and then facilitated microglial chemotaxis nearby for clearance. Simultaneously, Tf-Pep63-Lip hindered Aβ1-42 aggregation and disaggregated Aβ1-42 assembly due to multivalent PA-Aβ. Pep63 effectively inhibited the binding between EphB2 and Aβ oligomers after release from liposomes and rescued NMDA receptors trafficking, the basis of synaptic plasticity. No side effects were observed in either APP/PS1 or wild-type mice, indicating that Tf-Pep63-Lip might be safe under the dosing regimen used in our experiment. Taken together, our results suggested that Tf-Pep63-Lip may serve as a safe and efficient agent for AD combination therapy.
Identifiers
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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.