ArticleNature communications2024
β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer's Disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Apolipoprotein D acts as a chaperone of Aβ peptide delaying its assembly into amyloid aggregates.Cellular and molecular life sciences : CMLS · 2026Article
- Maintaining and regaining episodic memory in Alzheimer disease: a circuit-based perspective.Nature reviews. Neurology · 2026Review
- Microglial metabolic reprogramming drives the therapeutic effects of bavachinin on brain network function and memory in Alzheimer's disease.Frontiers in pharmacology · 2026Article
- The medial septum-hippocampus-lateral septum circuitry in spatial memory: linking healthy function to early Alzheimer's disease and translational opportunities.Translational neurodegeneration · 2025Review
- Amyloid β-dependent neuronal silencing through synaptic decoupling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Withaferin A Rescues Brain Network Dysfunction and Cognitive Deficits in a Mouse Model of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The Impact of the Exposome on Alzheimer's Disease: The Influence of Nutrition.International journal of molecular sciences · 2025Review
- Design of a ligand-dependent fluorescent biosensor, based on an engineered lipocalin (anticalin), for the sensitive detection of the Alzheimer β-amyloid peptide.Protein engineering, design & selection : PEDS · 2025Article
- Cholinergic Reinforcement Signaling Is Impaired by Amyloidosis Prior to Its Synaptic Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Hyperactivity mediated by synaptotoxic β-amyloid (Aβ) oligomers is one of the earliest forms of neuronal dysfunction in Alzheimer's disease. In the search for a preventive treatment strategy, we tested the effect of scavenging Aβ peptides before Aβ plaque formation. Using in vivo two-photon calcium imaging and SF-iGluSnFR-based glutamate imaging in hippocampal slices, we demonstrate that an Aβ binding anticalin protein (Aβ-anticalin) can suppress early neuronal hyperactivity and synaptic glutamate accumulation in the APP23xPS45 mouse model of β-amyloidosis. Our results suggest that the sole targeting of Aβ monomers is sufficient for the hyperactivity-suppressing effect of the Aβ-anticalin at early disease stages. Biochemical and neurophysiological analyses indicate that the Aβ-anticalin-dependent depletion of naturally secreted Aβ monomers interrupts their aggregation to neurotoxic oligomers and, thereby, reverses early neuronal and synaptic dysfunctions. Thus, our results suggest that Aβ monomer scavenging plays a key role in the repair of neuronal function at early stages of AD.
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