Authors: Yunjung Jin, Fuyao Li, Zonghua Li, Tadafumi C. Ikezu, Justin O’Leary, Manikandan Selvaraj, Yiyang Zhu , Yuka A. Martens, Shunsuke Koga, Hannah Santhakumar, Yonghe Li , Wenyan Lu, Yang You, Kiara Lolo, Michael DeTure, Alexandra I. Beasley, Mary D. Davis, Pamela J. McLean, Owen A. Ross, Takahisa Kanekiyo, Tsuneya Ikezu, Thomas Caulfield, Jonathan Carr, Zbigniew K. Wszolek, Guojun Bu, Dennis W. Dickson, and Na Zhao
Science Advances, 11 September 2024
Scientists use Axion’s Maestro Pro MEA to investigate neuronal pathology in iPSC-derived SCNA triplication cortical organoids.
Alpha-synuclein (a-syn) aggregation is a hallmark of Lewy body diseases (LBD), including Parkinson's disease and dementias, but the pathological mechanisms of a-Syn aggregation in cortical neurons remains unclear. In this study, researchers used human iPSC-derived cortical organoids generated from patients with LBD with SNCA gene triplications to investigate a-Syn pathology and assess FDA-approved drugs as potential therapeutics. To evaluate deficits in synaptogenesis (identified by RNA sequencing) in the organoids, the team used Axion’s noninvasive Maestro Pro multielectrode array (MEA) system. The results demonstrated that SNCA-mutant neurons exhibited decreased activity, supporting potential impaired synaptogenesis and neuronal pathology. Overall, the authors conclude that “the findings establish human cortical LBD models and suggest potential therapeutic drugs targeting α-SYN aggregation for LBD.”
