ReviewParkinsonism & related disorders2012
Genetic mouse models for understanding LRRK2 biology, pathology and pre-clinical application.
Review in Parkinsonism & related disorders, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 11 citations in OpenAlex.
- ASO-mediated knockdown or kinase inhibition ofMolecular therapy. Nucleic acids · 2023Article
- Age- and Sex-Dependent Behavioral and Neurochemical Alterations in hLRRK2-G2019S BAC Mice.Biomolecules · 2022Article
- Article
- Chronic MPTP administration regimen in monkeys: a model of dopaminergic and non-dopaminergic cell loss in Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Selective expression of Parkinson's disease-related Leucine-rich repeat kinase 2 G2019S missense mutation in midbrain dopaminergic neurons impairs dopamine release and dopaminergic gene expression.Human molecular genetics · 2015Article
- LRRKing up the right trees? On figuring out the effects of mutant LRRK2 and other Parkinson's disease-related genes.Basal ganglia · 2013Article
- Comprehensive characterization and optimization of anti-LRRK2 (leucine-rich repeat kinase 2) monoclonal antibodies.The Biochemical journal · 2013Article
- Current understanding of LRRK2 in Parkinson's disease: biochemical and structural features and inhibitor design.Future medicinal chemistry · 2012Review
- Small molecule kinase inhibitors for LRRK2 and their application to Parkinson's disease models.ACS chemical neuroscience · 2012Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Missense mutations in Leucine-Rich Repeat kinase 2 (LRRK2) are the most common cause of inherited Parkinson's disease (PD). Elucidation of LRRK2 biology and pathophysiology is central to the development of therapeutic intervention. Our group and others have developed a number of genetic mouse models of LRRK2 utilizing different genetic approaches. These models exhibit certain PD-related pathologies (e.g. impaired dopamine transmission and tauopathies) and abnormal motor functions, providing valuable insight into potential LRRK2-mediated pathogenesis of PD. However, not surprisingly they lack of substantial neuropathology and clinical syndromes of PD. Ongoing investigation of these models has begun to shed light on LRRK2 cellular functions and pathogenic pathways and is expected to assist the identification and validation of PD drug targets. This report summarizes the recent findings in our genetic LRRK2 models and discusses their utility in understanding much needed knowledge regarding early stage (pre-symptomatic) disease progression, drug target identification, and potential application in chemical screening focused on inhibitors of kinase activity of LRRK2.
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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.