Signaling pathways involved in 1-octen-3-ol mediated neurotoxicity in Drosophila melanogaster: Implication in Parkinsons Disease. Arati A. Inamdar, Joan W. Bennett. Department of Plant Biology and Pathology, Rutgers, The State University of New Jersey, New Brunswick, NJ.

   The prevalence and growing incidence of PD point to the accountability of other environmental risk factors for the pathogenesis of PD. In addition to the existing neurotoxin, recently, natural toxins have been reported to be the causative agents for PD. Our lab reported the deregulation of dopamine homeostasis by newly reported natural toxin, 1-octen-3-ol. 1-octen-3-ol is a fungal VOC known to be emitted by all fungi. Fungal exposure leads to neurological and neuropsychiatric problems such as movement disorders, delirium, dementia, and disorders of balance and coordination in human populations. We have pioneered Drosophila melanogasteras a reductionist model to determine the mechanism of toxicity of 1-octen-3-ol which has shown to cause loss of dopaminergic neurons and PD like symptoms in flies. In this report, we have incorporated our inexpensive Drosophila model as an in vivo genetic model to identify the modulatory role of JNK and Akt signaling pathways in 1-octen-3-ol induced dopamine neurotoxicity. We found that AKt and JNK protect against 1-octen-3-ol mediated dopamine toxicity. Hence, our Drosophila model system allows unique opportunity to screen for the relevant signaling pathways involved in 1-octen-3-ol and other fungal VOCs mediated toxicity.