ArticleHuman molecular genetics2013
Dopaminergic expression of the Parkinsonian gene LRRK2-G2019S leads to non-autonomous visual neurodegeneration, accelerated by increased neural demands for energy.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Lysosomal TPC2 channels disrupt Ca2+ entry and dopaminergic function in models of LRRK2-Parkinson's disease.The Journal of cell biology · 2025Article
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- Exploring LRRK2-dependent Mechanisms in Parkinson's Disease Therapy.CNS & neurological disorders drug targets · 2025Review
- Knocking out the LRRK2 gene increases sensitivity to wavelength information in rats.Scientific reports · 2024Article
- Review
- Human Induced Pluripotent Stem Cell Phenotyping and Preclinical Modeling of Familial Parkinson's Disease.Genes · 2022Review
- Choroid and choriocapillaris changes in early-stage Parkinson's disease: a swept-source optical coherence tomography angiography-based cross-sectional study.Alzheimer's research & therapy · 2022Article
- Presynaptic accumulation of α-synuclein causes synaptopathy and progressive neurodegeneration inBrain communications · 2021Article
- Retinal Degeneration: A Window to Understand the Origin and Progression of Parkinson's Disease?Frontiers in neuroscience · 2021Review
- Multiple Pathways of LRRK2-G2019S/Rab10 Interaction in Dopaminergic Neurons.Journal of Parkinson's disease · 2021Article
- Review
- Article
- Dopamine, Alpha-Synuclein, and Mitochondrial Dysfunctions in Parkinsonian Eyes.Frontiers in neuroscience · 2020Review
- Progress inFrontiers in neuroscience · 2020Review
- Lessons on Differential Neuronal-Death-Vulnerability from Familial Cases of Parkinson's and Alzheimer's Diseases.International journal of molecular sciences · 2019Review
- Female Genetic Contributions to Sperm Competition inGenetics · 2019Article
- Vitamin BCell research · 2019Article
- LRRK2 and mitochondria: Recent advances and current views.Brain research · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is associated with loss of dopaminergic signalling, and affects not just movement, but also vision. As both mammalian and fly visual systems contain dopaminergic neurons, we investigated the effect of LRRK2 mutations (the most common cause of inherited PD) on Drosophila electroretinograms (ERGs). We reveal progressive loss of photoreceptor function in flies expressing LRRK2-G2019S in dopaminergic neurons. The photoreceptors showed elevated autophagy, apoptosis and mitochondrial disorganization. Head sections confirmed extensive neurodegeneration throughout the visual system, including regions not directly innervated by dopaminergic neurons. Other PD-related mutations did not affect photoreceptor function, and no loss of vision was seen with kinase-dead transgenics. Manipulations of the level of Drosophila dLRRK suggest G2019S is acting as a gain-of-function, rather than dominant negative mutation. Increasing activity of the visual system, or of just the dopaminergic neurons, accelerated the G2019S-induced deterioration of vision. The fly visual system provides an excellent, tractable model of a non-autonomous deficit reminiscent of that seen in PD, and suggests that increased energy demand may contribute to the mechanism by which LRRK2-G2019S causes neurodegeneration.
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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.