ArticleJournal of cellular and molecular medicine2019
Levetiracetam treatment ameliorates LRRK2 pathological mutant phenotype.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Modelling Neural Disorders with theBiomolecules · 2025Review
- Identification of plasma exosomal microRNAs and bioinformatics analysis of the microRNA-messenger RNA regulatory pathways in mice with status epilepticus.Cytotechnology · 2025Article
- Review
- Evaluation of Neuroinflammatory Contribution to Neurodegeneration in LRRK2Biomedicines · 2024Article
- Inhibition of the Exocyst Complex Attenuates the LRRK2 Pathological Effects.International journal of molecular sciences · 2023Article
- Repositioning of drugs for Parkinson's disease and pharmaceutical nanotechnology tools for their optimization.Journal of nanobiotechnology · 2022Review
- Levetiracetam Mechanisms of Action: From Molecules to Systems.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Article
- Levetiracetam treatment ameliorates LRRK2 pathological mutant phenotype.Journal of cellular and molecular medicine · 2019Article
- Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease (PD). The LRRK2 physiological and pathological function is still debated. However, different experimental evidence based on LRRK2 cellular localization and LRRK2 protein interactors suggests that LRRK2 may be part and regulate a protein network modulating vesicle dynamics/trafficking. Interestingly, the synaptic vesicle protein SV2A is part of this protein complex. Importantly, SV2A is the binding site of the levetiracetam (LEV), a compound largely used in human therapy for epilepsy treatment. The binding of LEV to SV2A reduces the neuronal firing by the modulation of vesicle trafficking although by an unclear molecular mechanism. In this short communication, we have analysed the interaction between the LRRK2 and SV2A pathways by LEV treatment. Interestingly, LEV significantly counteracts the effect of LRRK2 G2019S pathological mutant expression in three different cellular experimental models. Our data strongly suggest that LEV treatment may have a neuroprotective effect on LRRK2 pathological mutant toxicity and that LEV repositioning could be a viable compound for PD treatment.
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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.