Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Glia are critical for the neuropathology of complex I deficiency in Drosophila.

Human molecular genetics - 1 Sept 2014

Hegde Vijay R, Vogel Rutger, Feany Mel B

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Drosophila melanogaster
Share to Electron Transport Complex I
Share to Gene Knockdown Techniques

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Mitochondria

Share to Mitochondrial Function and Pathology

Share to Neuroglia

Share to Neurotoxins

Share to Phenotype

Source

Open in PubMed Open full text

Identifiers

PMID: 24760769
DOI: 10.1093/hmg/ddu188
PMCID: PMC4119418

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Glia are critical for the neuropathology of complex I deficiency in Drosophila.PMID 24760769Read ↗

Modulating glial genes involved in synaptic function mitigates pathogenesis and behavioral deficits in a <i>Drosophila</i> model of Huntington’s DiseaseSemantic proximity Read ↗

Increased energy metabolism rescues glia-induced pathology in a Drosophila model of Huntington's diseaseSemantic proximity Read ↗

Yeast NDI1 expression prevents the unfolded protein response and reconfigures metabolism to restore neuronal function in mitochondrial complex I deficiencySemantic proximity Read ↗

A <i>Drosophila</i> model of mitochondrial disease phenotypic heterogeneitySemantic proximity Read ↗

Reactive oxygen species act remotely to cause synapse loss in a Drosophila model of developmental mitochondrial encephalopathy.Semantic proximity Read ↗

PARKINSON’S DISEASE-ASSOCIATED <i>PINK1</i> LOSS DISRUPTS ENSHEATHING GLIA AND CAUSES DOPAMINERGIC NEURON SYNAPSE LOSSSemantic proximity Read ↗

A Drosophila model of mitochondrial disease phenotypic heterogeneity.Semantic proximity Read ↗

Maintaining the brain: insight into human neurodegeneration from Drosophila melanogaster mutants.Semantic proximity Read ↗

Pathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency.Semantic proximity Read ↗

Downregulation of glial genes involved in synaptic function mitigates Huntington's disease pathogenesis.Semantic proximity Read ↗

Unraveling Novel Mechanisms of Neurodegeneration Through a Large-Scale Forward Genetic Screen in DrosophilaSemantic proximity Read ↗

A mutation in Drosophila Aldolase causes temperature-sensitive paralysis, shortened lifespan, and neurodegeneration.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.