ReviewFrontiers in cellular neuroscience2020
From Synaptic Dysfunction to Neuroprotective Strategies in Genetic Parkinson's Disease: Lessons From LRRK2.
Review in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Synapses-associated research in Parkinson's disease: an explored trends analysis.Frontiers in aging neuroscience · 2025Article
- The senescent synapse: A look at autophagy, calcium handling, and mitochondrial bioenergetics at the synapse in ageing and Parkinson's disease.Current research in physiology · 2025Review
- Neuroprotective Effects of the Nutraceutical Dehydrozingerone and Its CBiomolecules · 2024Article
- The genomic landscape of pediatric renal cell carcinomas.iScience · 2022Article
- Age-related LRRK2 G2019S Mutation Impacts Microglial Dopaminergic Fiber Refinement and Synaptic Pruning Involved in Abnormal Behaviors.Journal of molecular neuroscience : MN · 2022Article
- Update on CSF Biomarkers in Parkinson's Disease.Biomolecules · 2022Review
- Monogenetic Forms of Parkinson's Disease - Bridging the Gap Between Genetics and Biomarkers.Frontiers in aging neuroscience · 2022Review
- Future Prospects in Parkinson's Disease Diagnosis and Treatment.Noro psikiyatri arsivi · 2022Review
- Synaptic Dysfunction in Multiple Sclerosis: A Red Thread from Inflammation to Network Disconnection.International journal of molecular sciences · 2021Review
- Oxidative stress factors in Parkinson's disease.Neural regeneration research · 2021Review
- Molecular Mechanisms Underlying Synaptic and Axon Degeneration in Parkinson's Disease.Frontiers in cellular neuroscience · 2021Article
- Development of α-Synuclein Real-Time Quaking-Induced Conversion as a Diagnostic Method for α-Synucleinopathies.Frontiers in aging neuroscience · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The pathogenesis of Parkinson's disease (PD) is thought to rely on a complex interaction between the patient's genetic background and a variety of largely unknown environmental factors. In this scenario, the investigation of the genetic bases underlying familial PD could unveil key molecular pathways to be targeted by new disease-modifying therapies, still currently unavailable. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are responsible for the majority of inherited familial PD cases and can also be found in sporadic PD, but the pathophysiological functions of LRRK2 have not yet been fully elucidated. Here, we will review the evidence obtained in transgenic LRRK2 experimental models, characterized by altered striatal synaptic transmission, mitochondrial dysfunction, and α-synuclein aggregation. Interestingly, the processes triggered by mutant LRRK2 might represent early pathological phenomena in the pathogenesis of PD, anticipating the typical neurodegenerative features characterizing the late phases of the disease. A comprehensive view of LRRK2 neuronal pathophysiology will support the possible clinical application of pharmacological compounds targeting this protein, with potential therapeutic implications for patients suffering from both familial and sporadic PD.
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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.