| dc.contributor | Rosales-Corral, S.A., Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, United States, División Neurociencias, Centro de Investigación Biomédica de Occidente, Instituto Mexicano Del Seguro Social, Sierra Mojada 800 Col. Independencia, 44340 Guadalajara JAL, Mexico; Lopez-Armas, G., División Neurociencias, Centro de Investigación Biomédica de Occidente, Instituto Mexicano Del Seguro Social, Sierra Mojada 800 Col. Independencia, 44340 Guadalajara JAL, Mexico; Cruz-Ramos, J., División Neurociencias, Centro de Investigación Biomédica de Occidente, Instituto Mexicano Del Seguro Social, Sierra Mojada 800 Col. Independencia, 44340 Guadalajara JAL, Mexico; Melnikov, V.G., University Center for Biomedical Research Center, University of Colima, Colima, COL, Mexico; Tan, D.-X., Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, United States; Manchester, L.C., Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, United States; Munoz, R., Departamento de Química, Centro de Ciencias Exactas e Ingenieria (CUCEI), Universidad de Guadalajara, Blvd. Marcelino García Barragan 1421, 44430 Guadalajara JAL, Mexico; Reiter, R.J., Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229, United States | |
| dc.description.abstract | Alzheimer pathogenesis involves mitochondrial dysfunction, which is closely related to amyloid-? (A?) generation, abnormal tau phosphorylation, oxidative stress, and apoptosis. Alterations in membranal components, including cholesterol and fatty acids, their characteristics, disposition, and distribution along the membranes, have been studied as evidence of cell membrane alterations in AD brain. The majority of these studies have been focused on the cytoplasmic membrane; meanwhile the mitochondrial membranes have been less explored. In this work, we studied lipids and mitochondrial membranes in vivo, following intracerebral injection of fibrillar amyloid-? (A?). The purpose was to determine how A? may be responsible for beginning of a vicious cycle where oxidative stress and alterations in cholesterol, lipids and fatty acids, feed back on each other to cause mitochondrial dysfunction. We observed changes in mitochondrial membrane lipids, and fatty acids, following intracerebral injection of fibrillar A? in aged Wistar rats. Melatonin, a well-known antioxidant and neuroimmunomodulator indoleamine, reversed some of these alterations and protected mitochondrial membranes from obvious damage. Additionally, melatonin increased the levels of linolenic and n-3 eicosapentaenoic acid, in the same site where amyloid ? was injected, favoring an endogenous anti-inflammatory pathway Zapotitlán Copyright 2012 Sergio A. Rosales-Corral et al. | |
