ArticleHuman molecular genetics2014
Glia are critical for the neuropathology of complex I deficiency in Drosophila.
Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Quantitative In Vivo Imaging of ATP Dynamics in Drosophila Using the Ratiometric Biosensor QUEEN.Development, growth & differentiation · 2026Article
- Pathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency.Human molecular genetics · 2024Article
- A Drosophila model of mitochondrial disease phenotypic heterogeneity.Biology open · 2024Article
- A Drosophila model relevant to chemotherapy-related cognitive impairment.Scientific reports · 2023Article
- Integrative analysis reveals a conserved role for the amyloid precursor protein in proteostasis during aging.Nature communications · 2023Article
- Yeast NDI1 reconfigures neuronal metabolism and prevents the unfolded protein response in mitochondrial complex I deficiency.PLoS genetics · 2023Article
- Mitochondrial Neurodegeneration: Lessons fromBiomolecules · 2023Review
- Transcriptome Profiling of the Liver in Nellore Cattle Phenotypically Divergent for RFI in Two Genetic Groups.Animals : an open access journal from MDPI · 2023Article
- Eosin whole-brain mount staining to analyze neurodegeneration in a fly model of Alzheimer's disease.STAR protocols · 2022Article
- Roles for Mitochondrial Complex I Subunits in Regulating Synaptic Transmission and Growth.Frontiers in neuroscience · 2022Article
- Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020Review
- Downregulation of respiratory complex I mediates major signalling changes triggered by TOR activation.Scientific reports · 2020Article
- Insights from Drosophila on mitochondrial complex I.Cellular and molecular life sciences : CMLS · 2020Review
- Article
- AFrontiers in genetics · 2019Article
- Article
- A Conserved Cytoskeletal Signaling Cascade Mediates Neurotoxicity of FTDP-17 Tau MutationsThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Defective Phagocytic Corpse Processing Results in Neurodegeneration and Can Be Rescued by TORC1 Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial electron transport chain (ETC) disorders cause severe neurological disease, typically in the context of fatal encephalomyelopathies. Neuronal cell autonomous energy deficiency due to reduced mitochondrial adenosine triphosphate production is currently the leading hypothesis to explain the neurotoxicity in ETC disorders. To define the mechanisms underlying neuropathology in ETC disorders, we have modeled the most common type of ETC disorder, complex I deficiency, in Drosophila. Our model recapitulates important clinical features of the disease including neuronal loss, mitochondrial enlargement, motor dysfunction and early death. Using cell-type specific gene knockdown, we find that both neurons and glia contribute to the disease phenotype and that glia play a critical non-cell autonomous role in the development of neuronal toxicity. Our results open up an unexpected avenue of research, and could lead to the development of new treatment strategies.
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