ArticleScientific reports2018
Mutations in the Drosophila homolog of human PLA2G6 give rise to age-dependent loss of psychomotor activity and neurodegeneration.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Decanoic acid extends lifespan and modulates metabolism in models of PLA2G6-associated neurodegeneration.Disease models & mechanisms · 2025Article
- Natural variation in phospholipase IPLA2-VIA contributes to starvation sensitivity inbioRxiv : the preprint server for biology · 2025Article
- Altered Mitochondrial Bioenergetics and Calcium Kinetics in Young-Onset PLA2G6 Parkinson's Disease iPSCs.Journal of neurochemistry · 2025Article
- Ferroptosis role in complexity of cell death: unrevealing mechanisms in Parkinson's disease and therapeutic approaches.Inflammopharmacology · 2025Review
- Moxibustion inhibits inflammation in monosodium urate crystal-induced gouty arthritis model rats through metabolomic regulation.Frontiers in molecular biosciences · 2025Article
- GABAergic neurons are a key cell type in aFrontiers in neuroscience · 2025Article
- Investigating the mechanisms of resveratrol in the treatment of gouty arthritis through the integration of network pharmacology and metabolics.Frontiers in endocrinology · 2024Article
- Modeling Myotonic Dystrophy Type 2 UsingInternational journal of molecular sciences · 2023Review
- The Therapeutic Effect and the Potential Mechanism of Flavonoids and Phenolics ofMolecules (Basel, Switzerland) · 2022Article
- Cerebral Iron Deposition in Neurodegeneration.Biomolecules · 2022Review
- Molecular Characterization of Two Genes Encoding Novel CaCurrent issues in molecular biology · 2022Article
- The Importance ofCells · 2021Review
- iPLA2-VIA is required for healthy aging of neurons, muscle, and the female germline in Drosophila melanogaster.PloS one · 2021Article
- Pluripotent Stem Cell Derived Neurons as In Vitro Models for Studying Autosomal Recessive Parkinson's Disease (ARPD): PLA2G6 and Other Gene Loci.Advances in experimental medicine and biology · 2021Article
- Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA).Antioxidants (Basel, Switzerland) · 2020Review
- Overdosing on iron: Elevated iron and degenerative brain disorders.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Oxalate-Degrading Bacillus subtilis Mitigates Urolithiasis in a Drosophila melanogaster Model.mSphere · 2020Article
- Article
- iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- PLA2G6-Associated Neurodegeneration (PLAN): Review of Clinical Phenotypes and Genotypes.Frontiers in neurology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Infantile neuroaxonal dystrophy (INAD) is a fatal neurodegenerative disorder that typically begins within the first few years of life and leads to progressive impairment of movement and cognition. Several years ago, it was shown that >80% of patients with INAD have mutations in the phospholipase gene, PLA2G6. Interestingly, mutations in PLA2G6 are also causative in two other related neurodegenerative diseases, atypical neuroaxonal dystrophy and Dystonia-parkinsonism. While all three disorders give rise to similar defects in movement and cognition, some defects are unique to a specific disorder. At present, the cellular mechanisms underlying PLA2G6-associated neuropathology are poorly understood and there is no cure or treatment that can delay disease progression. Here, we show that loss of iPLA2-VIA, the Drosophila homolog of PLA2G6, gives rise to age-dependent defects in climbing and spontaneous locomotion. Moreover, using a newly developed assay, we show that iPLA2-VIA mutants also display impairments in fine-tune motor movements, motor coordination and psychomotor learning, which are distinct features of PLA2G6-associated disease in humans. Finally, we show that iPLA2-VIA mutants exhibit increased sensitivity to oxidative stress, progressive neurodegeneration and a severely reduced lifespan. Altogether, these data demonstrate that Drosophila iPLA2-VIA mutants provide a useful model to study human PLA2G6-associated neurodegeneration.
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