ReviewTranslational neurodegeneration2022
LRRK2 mutant knock-in mouse models: therapeutic relevance in Parkinson's disease.
Review in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- The close relationship between a rare disease and a common disease: Case report of a patient with gaucher disease and parkinsonism.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons.Nature communications · 2026Article
- Neuroprotection of engineeredJournal of Zhejiang University. Science. B · 2026Article
- Time vortex: the circadian-dopaminergic dialogue in Parkinson's disease.NPJ Parkinson's disease · 2026Review
- Mitochondrial Proteins in Putative Neuron-Derived Plasma Exosomes Are Altered in Parkinson's Disease: An Exploratory Study.Molecular neurobiology · 2026Article
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Unraveling the intersection of aging and Parkinson's disease: a collaborative roadmap for advancing research models.NPJ Parkinson's disease · 2026Review
- The gut microbiome promotes mitochondrial respiration in the brain of a Parkinson's disease mouse model.NPJ Parkinson's disease · 2025Article
- Parkinson's disease mutant Miro1 causes mitochondrial dysfunction and dopaminergic neuron loss.Brain : a journal of neurology · 2025Article
- Leucine-rich repeat kinase 2 impairs the release sites of Parkinson's disease vulnerable dopamine axons.bioRxiv : the preprint server for biology · 2025Article
- Microglial dynamics and neuroinflammation in prodromal and early Parkinson's disease.Journal of neuroinflammation · 2025Review
- PD-linked LRRK2 G2019S mutation impairs astrocyte morphology and synapse maintenance via ERM hyperphosphorylation.bioRxiv : the preprint server for biology · 2025Article
- Environmental Factors Exacerbate Parkinsonian Phenotypes in an Asian-Specific Knock-In LRRK2 Risk Variant in Mice.International journal of molecular sciences · 2025Article
- Affective phenotypes in heterozygousFrontiers in genetics · 2025Article
- Loss of mitochondrial CaCell communication and signaling : CCS · 2024Article
- LRRK2 kinase inhibition protects against Parkinson's disease-associated environmental toxicants.Neurobiology of disease · 2024Article
- Modeling of age-related neurological disease: utility of zebrafish.Frontiers in aging neuroscience · 2024Review
- Human iPSC-derived microglia carrying the LRRK2-G2019S mutation show a Parkinson's disease related transcriptional profile and function.Scientific reports · 2023Article
- Modeling Parkinson's disease in LRRK2 rodents.Neuronal signaling · 2023Review
- Regional genetic correlations highlight relationships between neurodegenerative disease loci and the immune system.Communications biology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the leucine-rich repeat kinase 2 gene (LRRK2) are one of the most frequent genetic causes of both familial and sporadic Parkinson's disease (PD). Mounting evidence has demonstrated pathological similarities between LRRK2-associated PD (LRRK2-PD) and sporadic PD, suggesting that LRRK2 is a potential disease modulator and a therapeutic target in PD. LRRK2 mutant knock-in (KI) mouse models display subtle alterations in pathological aspects that mirror early-stage PD, including increased susceptibility of nigrostriatal neurotransmission, development of motor and non-motor symptoms, mitochondrial and autophagy-lysosomal defects and synucleinopathies. This review provides a rationale for the use of LRRK2 KI mice to investigate the LRRK2-mediated pathogenesis of PD and implications from current findings from different LRRK2 KI mouse models, and ultimately discusses the therapeutic potentials against LRRK2-associated pathologies in 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.