Scallop-derived plasmalogen attenuates amyloid beta-induced inflammation and apoptosis in SH-SY5Y cells

Backgrounds With an increase in the world’s aging population, candidate substances for the management of neurodegenerative diseases, including Alzheimer’s disease (AD), have received considerable attention. Amyloid beta (Aβ) peptide, the leading cause of AD, induces synaptic deficits, eventually leading to cognitive impairment. Plasmalogen is a subclass of glycerophospholipids containing a vinyl ether group in the glycerol backbone which has various efficacies. Objectives In this study, we investigated the mechanisms of scallop-derived plasmalogen (SPL) in neurotoxicity in human neurons, which remain incompletely understood. SH-SY5Y human neuroblastaoma cells were treated with Aβ 1–42, a major component of amyloid deposits in AD brains. Results SPL inhibited the phosphorylation of glycogen synthase kinase 3β and tau induced by Aβ. In addition, SPL decreased Aβ generation by downregulating the expression of amyloid precursor protein (APP) and beta-site APP cleaving enzyme 1. Furthermore, SPL suppressed the release of pro-inflammatory cytokines and expression of apoptotic proteins induced by Aβ. Conclusion Our study indicates that SPL would reduce Aβ-induced neurotoxicity associated with inflammation and apoptosis in human neuroblastoma cells.