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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.

Phospholipase D functional ablation has a protective effect in an Alzheimer’s disease Caenorhabditis elegans model