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J. Biol. Chem., Vol. 280, Issue 49, 41057-41068, December 9, 2005

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Peroxisomal Proliferation Protects from -Amyloid Neurodegeneration^*

Manuel J. Santos, Rodrigo A. Quintanilla, Andrés Toro, Rodrigo Grandy, Margarita C. Dinamarca, Juan A. Godoy, and Nibaldo C. Inestrosa1

From the Centro de Regulación Celular y Patología "Joaquín V. Luco," Instituto Milenio, Avenida Zanartu 1482, Santiago, Chile and Unidad de Bioquímica Celular y Genética, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Casilla 114-D, Santiago, Chile

Alzheimer disease is a neurodegenerative process that leads to severe cognitive impairment as a consequence of selective death of neuronal populations. The molecular pathogenesis of Alzheimer disease involves the participation of the -amyloid peptide (A) and oxidative stress. We report here that peroxisomal proliferation attenuated A-dependent toxicity in hippocampal neurons. Pretreatment with Wy-14.463 (Wy), a peroxisome proliferator, prevent the neuronal cell death and neuritic network loss induced by the A peptide. Moreover, the hippocampal neurons treated with this compound, showed an increase in the number of peroxisomes, with a concomitant increase in catalase activity. Additionally, we evaluate the Wy protective effect on -catenin levels, production of intracellular reactive oxygen species, cytoplasmic calcium uptake, and mitochondrial potential in hippocampal neurons exposed to H₂ O₂ and A peptide. Results show that the peroxisomal proliferation prevents -catenin degradation, reactive oxygen species production, cytoplasmic calcium increase, and changes in mitochondrial viability. Our data suggest, for the first time, a direct link between peroxisomal proliferation and neuroprotection from A-induced degenerative changes.

Received for publication, May 11, 2005 , and in revised form, September 9, 2005.

^* This work was supported by FONDAP Grant 13980001 and a grant from the Millennium Institute for Fundamental and Applied Biology. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: CRCP-Biomedical Center, P. Universidad Católica de Chile, Alameda 340, Santiago, Chile. Tel.: 56-2-6862724; Fax: 56-2-6862959; E-mail: ninestr{at}genes.bio.puc.cl.

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