ReviewBiology2020
Lymphocyte-Activation Gene 3 (LAG3) Protein as a Possible Therapeutic Target for Parkinson's Disease: Molecular Mechanisms Connecting Neuroinflammation to α-Synuclein Spreading Pathology.
Review in Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Neuroprotective effects of lixisenatide against propagation of α-synuclein pathology in Parkinson's disease.Neural regeneration research · 2026Article
- Microglial Lag3 Drives α-Synuclein-induced Neurotoxic Activated (A1) Astrocytes and Neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Microglia in the crosstalk between peripheral and central nervous systems in Parkinson's disease.Translational neurodegeneration · 2025Review
- VISTA Alleviates Microglia-Mediated Neuroinflammation After Cerebral Ischemia-Reperfusion Injury via Regulating ACOD1/Itaconic Acid Metabolism.Molecular neurobiology · 2025Article
- Identification of Key Active Constituents inInternational journal of molecular sciences · 2025Article
- Soluble lymphocyte activation gene-3 (sLAG3) and CD4/CD8 ratio dynamics as predictive biomarkers in patients undergoing immune checkpoint blockade for solid malignancies.British journal of cancer · 2024Article
- The involvement of α-synucleinopathy in the disruption of microglial homeostasis contributes to the pathogenesis of Parkinson's disease.Cell communication and signaling : CCS · 2024Review
- Microbiome-based therapies for Parkinson's disease.Frontiers in nutrition · 2024Review
- Post-inflammatory administration ofFASEB bioAdvances · 2023Article
- Promising biomarkers and therapeutic targets for the management of Parkinson's disease: recent advancements and contemporary research.Metabolic brain disease · 2023Review
- Searching for Biomarkers in the Blood of Patients at Risk of Developing Parkinson's Disease at the Prodromal Stage.International journal of molecular sciences · 2023Article
- Association between LAG3/CD4 gene variants and risk of Parkinson's disease.European journal of clinical investigation · 2022Article
- Cutting-Edge: Preclinical and Clinical Development of the First Approved Lag-3 Inhibitor.Cells · 2022Review
- Extracellular Alpha-Synuclein: Mechanisms for Glial Cell Internalization and Activation.Biomolecules · 2022Review
- Emerging Therapeutic Strategies for Parkinson's Disease and Future Prospects: A 2021 Update.Biomedicines · 2022Review
- Alpha-Synuclein Targeting Therapeutics for Parkinson's Disease and Related Synucleinopathies.Frontiers in neurology · 2022Review
- Novel Immune Checkpoints in Esophageal Cancer: From Biomarkers to Therapeutic Targets.Frontiers in immunology · 2022Review
- Seven mysteries of LAG-3: a multi-faceted immune receptor of increasing complexity.Immunotherapy advances · 2022Review
- Role of Liver Growth Factor (LGF) in Parkinson's Disease: Molecular Insights and Therapeutic Opportunities.Molecular neurobiology · 2021Review
- Understanding LAG-3 Signaling.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the most common neurodegenerative movement disorder without any objective biomarker available to date. Increasing evidence highlights the critical role of neuroinflammation, including T cell responses, and spreading of aggregated α-synuclein in PD progression. Lymphocyte-activation gene 3 (LAG3) belongs to the immunoglobulin (Ig) superfamily expressed by peripheral immune cells, microglia and neurons and plays a key role in T cell regulation. The role of LAG3 has been extensively investigated in several human cancers, whereas until recently, the role of LAG3 in the central nervous system (CNS) has been largely unknown. Accumulating evidence highlights the potential role of LAG3 in PD pathogenesis, mainly by binding to α-synuclein fibrils and affecting its endocytosis and intercellular transmission, which sheds more light on the connection between immune dysregulation and α-synuclein spreading pathology. Serum and cerebrospinal fluid (CSF) soluble LAG3 (sLAG3) levels have been demonstrated to be potentially associated with PD development and clinical phenotype, suggesting that sLAG3 could represent an emerging PD biomarker. Specific single nucleotide polymorphisms (SNPs) of the LAG3 gene have been also related to PD occurrence especially in the female population, enlightening the pathophysiological background of gender-related PD clinical differences. Given also the ongoing clinical trials investigating various LAG3-targeting strategies in human diseases, new opportunities are being developed for PD treatment research. In this review, we discuss recent preclinical and clinical evidence on the role of LAG3 in PD pathogenesis and biomarker potential, aiming to elucidate its underlying molecular mechanisms.
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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.