Abstract
Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play a central role in neuronal degeneration. CD40 expression was increased on cultured microglia treated with freshly solublized amyloid-β (Aβ, 500 nanomolar) and on microglia from a transgenic murine model of AD (Tg APP(sw),). Increased tumor necrosis factor α production and induction of neuronal injury occurred when Aβ-stimulated microglia were treated with CD40 ligand (CD40L). Microglia from Tg APP(sw) mice deficient for CD40L demonstrated reduction in activation, suggesting that the CD40-CD40L interaction is necessary for Aβ-induced microglial activation. Finally, abnormal tau phosphorylation was reduced in Tg APP(sw) animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.
Original language | English (US) |
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Pages (from-to) | 2352-2355 |
Number of pages | 4 |
Journal | Science |
Volume | 286 |
Issue number | 5448 |
DOIs | |
State | Published - Dec 17 1999 |
Externally published | Yes |
ASJC Scopus subject areas
- General