ArticleScientific reports2018
Phospholipase D functional ablation has a protective effect in an Alzheimer's disease Caenorhabditis elegans model.
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 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Exosome-Mediated Delivery of a PLD1 Modulator Overcomes Bioavailability Hurdles to Target Synaptopathy in Neurodegenerative Diseases.Pharmaceutical research · 2025Article
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- The Potential Mechanism of Eriodictyol in Treating Alzheimer's Disease: A Study on Computer-assisted Investigational Strategies.Current pharmaceutical design · 2024Article
- Phospholipase D, a Novel Therapeutic Target Contributes to the Pathogenesis of Neurodegenerative and Neuroimmune Diseases.Analytical cellular pathology (Amsterdam) · 2024Review
- The effect of lipid metabolism on age-associated cognitive decline: Lessons learned from model organisms and human.IBRO neuroscience reports · 2023Article
- Article
- Effects of APOE4 allelic dosage on lipidomic signatures in the entorhinal cortex of aged mice.Translational psychiatry · 2022Article
- Modeling Alzheimer's Disease inBiomedicines · 2022Review
- Evaluation of the silkwormRoyal Society open science · 2020Article
- Loss of egli-1, the Caenorhabditis elegans Orthologue of a Downstream Target of SMN, Leads to Abnormalities in Sensorimotor Integration.Molecular neurobiology · 2020Article
- Regulation of Membrane Turnover by Phosphatidic Acid: Cellular Functions and Disease Implications.Frontiers in cell and developmental biology · 2019Review
- Functional analysis of mammalian phospholipase D enzymes.Bioscience reports · 2018Article
- Presenilin mutations deregulate mitochondrial CaeLife · 2018Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Phospholipase D (PLD) is a key player in the modulation of multiple aspects of cell physiology and has been proposed as a therapeutic target for Alzheimer's disease (AD). Here, we characterize a PLD mutant, pld-1, using the Caenorhabditis elegans animal model. We show that pld-1 animals present decreased phosphatidic acid levels, that PLD is the only source of total PLD activity and that pld-1 animals are more sensitive to the acute effects of ethanol. We further show that PLD is not essential for survival or for the normal performance in a battery of behavioral tests. Interestingly, pld-1 animals present both increased size and lipid stores levels. While ablation of PLD has no important effect in worm behavior, its ablation in an AD-like model that overexpresses amyloid-beta (Aβ), markedly improves various phenotypes such as motor tasks, prevents susceptibility to a proconvulsivant drug, has a protective effect upon serotonin treatment and reverts the biometric changes in the Aβ animals, leading to the normalization of the worm body size. Overall, this work proposes the C. elegans model as a relevant tool to study the functions of PLD and further supports the notion that PLD has a significant role in neurodegeneration.
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