神经突
神经退行性变
高磷酸化
冈田酸
细胞生物学
神经科学
阿尔茨海默病
细胞
化学
生物
人口
神经元
体外
磷酸化
磷酸酶
生物化学
病理
医学
疾病
环境卫生
作者
Anja Kunze,Robert Meißner,Serena Brando,Philippe Renaud
摘要
This communication presents a novel experimental model for Alzheimer studies, where connected primary neurons were set into subtend, co-pathological states. Cortical neurons were cultured in two separated cell compartments in a microfluidic device. A neurite network was generated in a main channel through the neurite outgrowth from both cell compartments. A gradient of okadaic acid (OA) is generated over this neurite network by perfusion. OA is a phosphatase inhibitor that induces hyperphosphorylation of Tau proteins, a major hallmark in Alzheimer disease. The local OA treatment resulted in a connected "diseased" and "healthy" cell population. Anti-phosphorylated tau (Ser262) staining confirmed different states of phosphorylated Tau proteins, and synapthophysin staining the connection of "healthy" and "diseased" cells. Here, we present a novel in vitro model that opens the possibility to study cellular and molecular propagation mechanisms in neurodegeneration, in Tauopathies (as e.g., in Alzheimer), as well as simultaneous drug effects on connected healthy and diseased cell populations.
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