ArticleBioEssays : news and reviews in molecular, cellular and developmental biology2010
Mechanisms in dominant parkinsonism: The toxic triangle of LRRK2, alpha-synuclein, and tau.
Article in BioEssays : news and reviews in molecular, cellular and developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 70 citations in OpenAlex.
- Review
- Association betweenFrontiers in genetics · 2025Article
- Protein Translation in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- Pathogenic LRRK2 requires secondary factors to induce cellular toxicity.Bioscience reports · 2020Article
- The Diverse Roles of TAO Kinases in Health and Diseases.International journal of molecular sciences · 2020Review
- The role of posttranslational modifications of α-synuclein and LRRK2 in Parkinson's disease: Potential contributions of environmental factors.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Cryo-EM analysis of homodimeric full-length LRRK2 and LRRK1 protein complexes.Scientific reports · 2017Article
- Back to the tubule: microtubule dynamics in Parkinson's disease.Cellular and molecular life sciences : CMLS · 2017Review
- Current Opinion on the Role of Neurogenesis in the Therapeutic Strategies for Alzheimer Disease, Parkinson Disease, and Ischemic Stroke; Considering Neuronal Voiding Function.International neurourology journal · 2016Review
- Genes associated with Parkinson's disease: regulation of autophagy and beyond.Journal of neurochemistry · 2016Review
- LRRK2 Promotes Tau Accumulation, Aggregation and Release.Molecular neurobiology · 2016Article
- Regulation of LRRK2 promoter activity and gene expression by Sp1.Molecular brain · 2016Article
- Neurite Aggregation and Calcium Dysfunction in iPSC-Derived Sensory Neurons with Parkinson's Disease-Related LRRK2 G2019S Mutation.Stem cell reports · 2015Article
- LRRK2 Pathways Leading to Neurodegeneration.Current neurology and neuroscience reports · 2015Review
- Interaction between SNCA, LRRK2 and GAK increases susceptibility to Parkinson's disease in a Chinese population.eNeurologicalSci · 2015Article
- Glutaredoxin deficiency exacerbates neurodegeneration in C. elegans models of Parkinson's disease.Human molecular genetics · 2015Article
- Genetic and pharmacological evidence that G2019S LRRK2 confers a hyperkinetic phenotype, resistant to motor decline associated with aging.Neurobiology of disease · 2014Article
- Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration.Biochimica et biophysica acta · 2014Article
- The regulation and deregulation of Wnt signaling by PARK genes in health and disease.Journal of molecular cell biology · 2014Review
- Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism.Frontiers in genetics · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is generally sporadic but a number of genetic diseases have parkinsonism as a clinical feature. Two dominant genes, alpha-synuclein (SNCA) and leucine-rich repeat kinase 2 (LRRK2), are important for understanding inherited and sporadic PD. SNCA is a major component of pathologic inclusions termed Lewy bodies found in PD. LRRK2 is found in a significant proportion of PD cases. These two proteins may be linked as most LRRK2 PD cases have SNCA-positive Lewy bodies. Mutations in both proteins are associated with toxic effects in model systems although mechanisms are unclear. LRRK2 is an intracellular signaling protein possessing both GTPase and kinase activities that may contribute to pathogenicity. A third protein, tau, is implicated as a risk factor for PD. We discuss the potential relationship between these genes and suggest a model for PD pathogenesis where LRRK2 is upstream of pathogenic effects through SNCA, tau, or both proteins.
Indexed as
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What OpenQuestion holds
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.