Get access

Co-pathological connected primary neurons in a microfluidic device for alzheimer studies

Authors

  • Anja Kunze,

    Corresponding author
    1. Laboratoire de Microsystèmes LMIS4, Ecole Polytechnique Fédérale de Lausanne, Station 17, CH-1015 Lausanne, Switzerland; telephone: +41-216936839; fax: +41-216935950
    • Laboratoire de Microsystèmes LMIS4, Ecole Polytechnique Fédérale de Lausanne, Station 17, CH-1015 Lausanne, Switzerland; telephone: +41-216936839; fax: +41-216935950.
    Search for more papers by this author
  • Robert Meissner,

    1. Laboratoire de Microsystèmes LMIS4, Ecole Polytechnique Fédérale de Lausanne, Station 17, CH-1015 Lausanne, Switzerland; telephone: +41-216936839; fax: +41-216935950
    Search for more papers by this author
  • Serena Brando,

    1. Laboratoire de Microsystèmes LMIS4, Ecole Polytechnique Fédérale de Lausanne, Station 17, CH-1015 Lausanne, Switzerland; telephone: +41-216936839; fax: +41-216935950
    Search for more papers by this author
  • Philippe Renaud

    1. Laboratoire de Microsystèmes LMIS4, Ecole Polytechnique Fédérale de Lausanne, Station 17, CH-1015 Lausanne, Switzerland; telephone: +41-216936839; fax: +41-216935950
    Search for more papers by this author

  • Anja Kunze and Robert Meissner contributed equally to this work.

Abstract

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. Biotechnol. Bioeng. 2011;108:2241–2245. © 2011 Wiley Periodicals, Inc.

Get access to the full text of this article

Ancillary