ArticleHuman molecular genetics2012
Rab11 rescues synaptic dysfunction and behavioural deficits in a Drosophila model of Huntington's disease.
Article in Human molecular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026Article
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- Downregulation of Pten Improves Huntington's Disease Phenotype by Reducing Htt Aggregates and Cell Death.Molecular neurobiology · 2025Article
- Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.CNS neuroscience & therapeutics · 2024Review
- Crosstalk between the Rho and Rab family of small GTPases in neurodegenerative disorders.Frontiers in cellular neuroscience · 2023Review
- Therapeutic Targeting of Rab GTPases: Relevance for Alzheimer's Disease.Biomedicines · 2022Review
- Glutamatergic Synapse Dysfunction inFrontiers in molecular neuroscience · 2022Article
- Synaptic Vesicle Recycling and the Endolysosomal System: A Reappraisal of Form and Function.Frontiers in synaptic neuroscience · 2022Review
- Cooperation of cell adhesion and autophagy in the brain: Functional roles in development and neurodegenerative disease.Matrix biology plus · 2021Review
- Article
- Vps54 Regulates Lifespan and Locomotor Behavior in AdultFrontiers in genetics · 2021Article
- Disruption of Tip60 HAT mediated neural histone acetylation homeostasis is an early common event in neurodegenerative diseases.Scientific reports · 2020Article
- Vps54 regulatesBiology open · 2020Article
- Excess Rab4 rescues synaptic and behavioral dysfunction caused by defective HTT-Rab4 axonal transport in Huntington's disease.Acta neuropathologica communications · 2020Article
- Autophagic and endo-lysosomal dysfunction in neurodegenerative disease.Molecular brain · 2019Review
- Rab GTPases: Switching to Human Diseases.Cells · 2019Review
- Tissue-Specific Upregulation of Drosophila Insulin Receptor (InR) Mitigates Poly(Q)-Mediated Neurotoxicity by Restoration of Cellular Transcription Machinery.Molecular neurobiology · 2019Article
- Article
- Rab GTPases and Membrane Trafficking in Neurodegeneration.Current biology : CB · 2018Review
- Critical importance of RAB proteins for synaptic function.Small GTPases · 2018Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Synapse abnormalities in Huntington's disease (HD) patients can precede clinical diagnosis and neuron loss by decades. The polyglutamine expansion in the huntingtin (htt) protein that underlies this disorder leads to perturbations in many cellular pathways, including the disruption of Rab11-dependent endosomal recycling. Impairment of the small GTPase Rab11 leads to the defective formation of vesicles in HD models and may thus contribute to the early stages of the synaptic dysfunction in this disorder. Here, we employ transgenic Drosophila melanogaster models of HD to investigate anomalies at the synapse and the role of Rab11 in this pathology. We find that the expression of mutant htt in the larval neuromuscular junction decreases the presynaptic vesicle size, reduces quantal amplitudes and evoked synaptic transmission and alters larval crawling behaviour. Furthermore, these indicators of early synaptic dysfunction are reversed by the overexpression of Rab11. This work highlights a potential novel HD therapeutic strategy for early intervention, prior to neuronal loss and clinical manifestation of disease.
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