Microglial Activation Resulting from CD40-CD40L Interaction After β-Amyloid Stimulation

• DOI: 10.1126/science.286.5448.2352
• Publication Date: 2002-07-27T09:42:47Z
• Authors: Jun Tan; Terrence Town; Daniel Paris; Takashi Mori; Zhiming Suo; Fiona Crawford; Mark P. Mattson; Richard A. Flavell; Michael Mullan
• Keywords: Pathogenesis; Amyloid (mycology)

Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play central role in neuronal degeneration. CD40 expression was increased on cultured treated with freshly solublized amyloid-β (Aβ, 500 nanomolar) from transgenic murine model of AD (Tg APP sw ). Increased tumor necrosis factor α production induction injury occurred when Aβ-stimulated were ligand (CD40L). Microglia Tg mice deficient for CD40L demonstrated reduction activation, suggesting that the CD40-CD40L interaction is necessary Aβ-induced microglial activation. Finally, abnormal tau phosphorylation reduced animals CD40L, an early event pathogenesis.