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The Journal of Neuroscience, February 18, 2004, 24(7):1760-1771; doi:10.1523/JNEUROSCI.4580-03.2004
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Cellular/Molecular
Tumor Necrosis Factor Death Receptor Signaling Cascade Is Required for Amyloid- Protein-Induced Neuron Death
Rena Li,2
Libang Yang,1
Kristina Lindholm,1
Yoshihiro Konishi,1
Xu Yue,2
Harald Hampel,3
Dai Zhang,4 and
Yong Shen1,5
1Haldeman Laboratory of Molecular and Cellular Neurobiology and 2L. J. Roberts Center for Alzheimer's Research, Sun Health Research Institute, Sun City, Arizona 85351, 3Department of Psychiatry, Ludwig-Maximilian University, 80336 Munich, Germany, 4Institute of Mental Health, Beijing University Medical School, Beijing, China, and 5Molecular and Cellular Biology Program, Arizona State University, Tempe, Arizona 85287
Tumor necrosis factor type I receptor (TNFRI), a death receptor, mediates apoptosis and plays a crucial role in the interaction between the nervous and immune systems. A direct link between death receptor activation and signal cascade-mediated neuron death in brains with neurodegenerative disorders remains inconclusive. Here, we show that amyloid- protein (A), a major component of plaques in the Alzheimer's diseased brain, induces neuronal apoptosis through TNFRI by using primary neurons overexpressing TNFRI by viral infection or neurons from TNFRI knock-out mice. This was mediated via alteration of apoptotic protease-activating factor (Apaf-1) expression that in turn induced activation of nuclear factor  B (NF-B). A-induced neuronal apoptosis was reduced with lower Apaf-1 expression, and little NF-B activation was found in the neurons with mutated Apaf-1 or a deletion of TNFRI compared with the cells from wild-type (WT) mice. Our studies suggest a novel neuronal response of A, which occurs through a TNF receptor signaling cascade and a caspase-dependent death pathway.
Key words: Alzheimer; apoptosis; death; degeneration; neuron; receptor
Received Oct 9, 2003;
revised December 30, 2003;
accepted January 3, 2004.
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