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The Journal of Neuroscience, 2001, 21:RC118:1-5

RAPID COMMUNICATION
Amyloid- Peptides Are Cytotoxic to Oligodendrocytes

Jan Xu, Shawei Chen, S. Hinan Ahmed, Hong Chen, Grace Ku, Mark P. Goldberg, and Chung Y. Hsu

Department of Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri 63110

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive dementia. Amyloid- peptide (A), a 39-43 amino acid peptide derived from -amyloid precursor protein, forms insoluble fibrillar aggregates that have been linked to neuronal and vascular degeneration in AD and cerebral amyloid angiopathy. Here we demonstrate that A 1-40 and a truncated fragment, A 25-35, induced death of oligodendrocytes (OLGs) in vitro in a dose-dependent manner with similar potencies. A-induced OLG death was accompanied by nuclear DNA fragmentation, mitochondrial dysfunction, and cytoskeletal disintegration. A activation of redox-sensitive transcription factors NF-B and AP-1 and antioxidant prevention of A-mediated OLG death suggest that oxidative injury contributes to A cytotoxicity in OLGs. Recent demonstration of A deposition and white matter abnormalities in AD implies a potential pathophysiological role for A-mediated cytotoxicity of OLGs in this neurodegenerative disease.

Key words: Alzheimer's disease; apoptosis; cell death; mitochondrial DNA; oxidative stress; white matter

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Copyright © 0000 Society for Neuroscience  0270-6474/00/$05.00/0

This article has been cited by other articles:

				K. J. Yin, J.-M. Lee, S. D. Chen, J. Xu, and C. Y. Hsu Amyloid-beta Induces Smac Release via AP-1/Bim Activation in Cerebral Endothelial Cells J. Neurosci., November 15, 2002; 22(22): 9764 - 9770. [Abstract] [Full Text] [PDF]

				P. Kienlen-Campard, S. Miolet, B. Tasiaux, and J.-N. Octave Intracellular Amyloid-beta 1-42, but Not Extracellular Soluble Amyloid-beta Peptides, Induces Neuronal Apoptosis J. Biol. Chem., May 3, 2002; 277(18): 15666 - 15670. [Abstract] [Full Text] [PDF]

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