Abstract
Soluble amyloid β1–42 (Aβ1–42) peptide has recently been assigned a key role in early Alzheimer’s disease (AD) pathophysiology accounting for synaptic dysfunction before amyloid plaque formation and neurodegeneration can occur. Following sublethal Aβ1–42 administration, we observed an acute but transient reduction of the spike and burst rate of spontaneously active cortical networks cultured on microelectrode arrays. This simple experimental system appears suitable for future long-term pharmacological and genetic studies of Aβ1–42 signaling, thus providing a valuable new tool in AD research.
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Acknowledgment
This study was supported by a grant from the Stiftung für Altersforschung (Age Research Foundation) of the Heinrich-Heine-Universität Düsseldorf (C.L.-A. and P.G.).
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Görtz, P., Opatz, J., Siebler, M. et al. Transient reduction of spontaneous neuronal network activity by sublethal amyloid β (1–42) peptide concentrations. J Neural Transm 116, 351–355 (2009). https://doi.org/10.1007/s00702-009-0188-y
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DOI: https://doi.org/10.1007/s00702-009-0188-y