ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Lymphocyte-Activation Gene 3 Facilitates Pathological Tau Neuron-to-Neuron Transmission.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 11 citations in OpenAlex.
- Retinal proteomics in neurodegeneration: Insights into ocular and brain disorders.Neural regeneration research · 2026Article
- Age-dependent transcriptomic effects of morphine in the frontal cortex of female mice.Neuropharmacology · 2026Article
- Microglial Lag3 Drives α-Synuclein-induced Neurotoxic Activated (A1) Astrocytes and Neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Incidental vs. Engineered Nanoparticles in Alzheimer's and Parkinson's Disease: Pathological Pathways and Therapeutic Interventions.Nano research · 2025Article
- Lewy body dementia promotion by air pollutants.Science (New York, N.Y.) · 2025Article
- TREM2 and LAG-3 in cancer and Alzheimer's disease immunotherapy.Trends in pharmacological sciences · 2025Review
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- Histogram-based analysis for confocal microscope images with immunofluorescent staining: A graphical-user-interface tool.MethodsX · 2025Article
- Proteomic signatures of corona and herpes viral antibodies identify IGDCC4 as a mediator of neurodegeneration.Science advances · 2025Article
- Divergent disruptive effects of soluble recombinant tau assemblies on synaptic plasticity in vivo.Molecular brain · 2025Article
- Emerging targets of α-synuclein spreading in α-synucleinopathies: a review of mechanistic pathways and interventions.Molecular neurodegeneration · 2025Review
- Neuronal LAG3 facilitates pathogenic α-synuclein neuron-to-neuron propagation.bioRxiv : the preprint server for biology · 2025Article
- Prion and "Prion-Like" Detection: From Conventional Methods to Microfluidics or Lab-on-Chip Platforms to Monitor Seeding and Spreading of Misfolded Proteins.Sub-cellular biochemistry · 2025Review
- Recent advances in therapeutic strategies for Alzheimer's and Parkinson's disease using protein/peptide co-modified polymer nanoparticles.Neuroprotection (Chichester, England) · 2024Review
- The cellular prion protein does not affect tau seeding and spreading of sarkosyl-insoluble fractions from Alzheimer's disease.Scientific reports · 2024Article
- Lymphocyte-Activation Gene 3 Facilitates Pathological Tau Neuron-to-Neuron Transmission.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Risk Factors and Diagnostic Model Construction of Chronic Pain with Cognitive Impairment.Journal of pain research · 2024Article
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30 authors at 5 institutions in 1 country.
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Abstract
The spread of prion-like protein aggregates is a common driver of pathogenesis in various neurodegenerative diseases, including Alzheimer's disease (AD) and related Tauopathies. Tau pathologies exhibit a clear progressive spreading pattern that correlates with disease severity. Clinical observation combined with complementary experimental studies has shown that Tau preformed fibrils (PFF) are prion-like seeds that propagate pathology by entering cells and templating misfolding and aggregation of endogenous Tau. While several cell surface receptors of Tau are known, they are not specific to the fibrillar form of Tau. Moreover, the underlying cellular mechanisms of Tau PFF spreading remain poorly understood. Here, it is shown that the lymphocyte-activation gene 3 (Lag3) is a cell surface receptor that binds to PFF but not the monomer of Tau. Deletion of Lag3 or inhibition of Lag3 in primary cortical neurons significantly reduces the internalization of Tau PFF and subsequent Tau propagation and neuron-to-neuron transmission. Propagation of Tau pathology and behavioral deficits induced by injection of Tau PFF in the hippocampus and overlying cortex are attenuated in mice lacking Lag3 selectively in neurons. These results identify neuronal Lag3 as a receptor of pathologic Tau in the brain，and for AD and related Tauopathies, a therapeutic target.
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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.