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Article Addendum
Increased Autophagic Degradation of Mitochondria in Alzheimer Disease
Paula I. Moreira, Sandra L. Siedlak, Xinglong Wang, Maria S. Santos, Catarina R. Oliveira, Massimo Tabaton, Akihiko Nunomura, Luke I. Szweda, Gjumrakch Aliev, Mark A. Smith, Xiongwei Zhu and George Perry
volume 3 | issue 6
November/December 2007Pages: 614 - 615
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Extensive literature exists supporting a role for mitochondrial dysfunction and oxidative damage in the pathogenesis of Alzheimer disease. Mitochondria are a major source of intracellular reactive oxygen species and are particularly vulnerable to oxidative stress. It has been recently shown that the immunoreactivity of lipoic acid and cytochrome oxidase-1, two mitochondrial markers, is increased in the cytoplasm of pyramidal neurons in Alzheimer disease cases compared with controls. Furthermore, lipoic acid was found to be strongly associated with granular structures and, by ultrastructure analysis, it was shown to be localized in mitochondria, cytosol and, importantly, in organelles identified as autophagic vacuoles. Lipoic acid was also found associated with the electron dense core of lipofuscin in the brains of Alzheimer disease cases but not in controls, whereas cytochrome oxidase-1 immunoreactivity was limited to mitochondria and cytosol in both Alzheimer and control cases. These data suggest that mitochondria are key targets of increased autophagic degradation in Alzheimer disease. The study of autophagy in Alzheimer disease could clarify the mechanisms underlying this neurodegenerative disorder and, eventually, help in the development of new therapeutic strategies.
Addendum to:
Autophagocytosis of Mitochondria is Prominent in Alzheimer Disease
Moreira PI, Siedlak SL, Wang X, Santos MS, Oliveira CR, Tabaton M, Nunomura A, Szweda LI, Aliev G, Smith MA, Zhu X and Perry G
J Neuropathol Exp Neurol 2007; 66:525-32
Authors
Paula I. Moreira
Center for Neuroscience and Cell Biology
Sandra L. Siedlak
Case Western Reserve University
Xinglong Wang
Case Western Reserve University
Maria S. Santos
University of Coimbra
Catarina R. Oliveira
University of Coimbra
Massimo Tabaton
University of Genoa
Akihiko Nunomura
Asahikawa Medical College
Luke I. Szweda
Oklahoma Medical Research Center
Gjumrakch Aliev
University of Texas at San Antonio
Mark A. Smith
Case Western Reserve University
Xiongwei Zhu
Case Western Reserve University
George Perry
University of Texas at San Antonio
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.