ArticleNeurobiology of aging2015
Behavioral, neurochemical, and pathologic alterations in bacterial artificial chromosome transgenic G2019S leucine-rich repeated kinase 2 rats.
Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 50 citations in OpenAlex.
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- Environmental Factors Exacerbate Parkinsonian Phenotypes in an Asian-Specific Knock-In LRRK2 Risk Variant in Mice.International journal of molecular sciences · 2025Article
- Behavioral analysis of motor and non-motor impairment in rodent models of Parkinson's disease.Frontiers in aging neuroscience · 2024Review
- The AAV-α-Synuclein Model of Parkinson's Disease: An Update.Journal of Parkinson's disease · 2024Review
- Modeling Parkinson's disease in LRRK2 rodents.Neuronal signaling · 2023Review
- Dopamine Transporter, PhosphoSerine129 α-Synuclein and α-Synuclein Levels in Aged LRRK2 G2019S Knock-In and Knock-Out Mice.Biomedicines · 2022Article
- Genetic background influences LRRK2-mediated Rab phosphorylation in the rat brain.Brain research · 2021Article
- Comprehensive Perspectives on Experimental Models for Parkinson's Disease.Aging and disease · 2021Review
- Current and Emerging MR Methods and Outcome in Rodent Models of Parkinson's Disease: A Review.Frontiers in neuroscience · 2021Review
- Pathogenic LRRK2 requires secondary factors to induce cellular toxicity.Bioscience reports · 2020Article
- PhIP exposure in rodents produces neuropathology potentially relevant to Alzheimer's disease.Toxicology · 2020Article
- Biological links between traumatic brain injury and Parkinson's disease.Acta neuropathologica communications · 2020Review
- Neuromelanin Modulates Heterocyclic Aromatic Amine-Induced Dopaminergic Neurotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- CAV-2-Mediated GFP and LRRK2Frontiers in molecular neuroscience · 2020Article
- Progress inFrontiers in neuroscience · 2020Review
- Leucine-rich repeat kinase-2 (LRRK2) modulates paraquat-induced inflammatory sickness and stress phenotype.Journal of neuroinflammation · 2019Article
- Alterations in the nigrostriatal dopamine system after acute systemic PhIP exposure.Toxicology letters · 2018Article
- New Developments in Genetic rat models of Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2018Review
- Probiotics Affect One-Carbon Metabolites and Catecholamines in a Genetic Rat Model of Depression.Molecular nutrition & food research · 2018Article
- Dopamine D2 receptor-mediated neuroprotection in a G2019S Lrrk2 genetic model of Parkinson's disease.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in leucine-rich repeated kinase 2 (LRRK2) cause autosomal dominant late-onset Parkinson's disease (PD), and the G2019S mutation in the kinase domain of LRRK2 is the most common genetic cause of familial PD. Enhanced kinase activity of G2019S LRRK2 is a suspected mechanism for carriers to develop PD but pathophysiological function of G2019S LRRK2 is not clear. The objective of the present study was to characterize a bacterial artificial chromosome rat expressing human G2019S LRRK2. Immunoblotting analysis showed that G2019S LRRK2 expression was approximately 5-8 times higher than wild-type rat LRRK2. At ages of 4, 8, and 12 months, our characterization showed that expression of G2019S LRRK2 induced oxidative stress in striatum and substantia nigra, increased inducible nitric oxide synthase expression in nigral dopamine neurons, and abnormal morphology of nigral dopaminergic neurons in transgenic rats compared with wild-type, without inducing overt neurodegeneration in nigrostriatal dopaminergic neurons. Thus, we conclude that although this model does not reproduce the key features of end-stage PD, important preclinical features of the disease are evident, which may be useful in studying the earliest stages of PD and for gene-environment interaction studies.
Indexed as
Identifiers
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.