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Endoplasmic reticulum (ER) and mitochondria are distributed in close communication via a dynamic ER-calcium (Ca2+) mitochondria interconnection and regulate a plethora of vital cellular functions, including Ca2+ homeostasis, mitochondrial transport and dynamics, bioenergetics, ER stress, apoptotic signaling, and inflammation (Erpapazoglou et al., 2017). Alteration in the ER-mitochondria communication adversely affects overall physiology of the cell (Gómez-Suaga et al., 2018). ER-mitochondria communication is also involved in lipid transport, suggesting that lipidomic approach may be useful to study the potential mechanisms leading to impaired neuropeptidergic signaling (Valadas et al., 2018). Mitochondria-associated membranes (MAMs) are defined as specialized subdomains connecting ER and mitochondria in order to regulate physiological functions, maintain Ca2+ signaling and other vital cellular processes (Rodríguez-Arribas et al., 2017). Neurons are highly dependent on MAMs to exchange metabolites and signaling molecules between ER and mitochondria, suggesting that altered function of MAMs due to toxin insults such as rotenone and manganese could play a crucial role in the pathogenesis of neurodegenerative diseases, including Parkinson’s disease (PD)(Krols et al., 2016; Harischandra et al.; Ramalingam et al.; Valdinocci et al.). Modifications in the communication between ER and mitochondria cause a reduction in mitochondrial Ca2+ homeostasis in several animal models of neurodegeneration, such as PD, an age-dependent neurodegenerative disorder characterized by the progressive loss of dopamine (DA …