The Catalytically Active Copper-Amyloid-Beta State: Coordination Site Responsible for Reactive Oxygen Species Production

2013 ◽  
Vol 125 (42) ◽  
pp. 11316-11319 ◽  
Author(s):  
Laure-Estelle Cassagnes ◽  
Vincent Hervé ◽  
Françoise Nepveu ◽  
Christelle Hureau ◽  
Peter Faller ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Amyloid Beta ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Coordination Site ◽  
Catalytically Active ◽  
State Coordination ◽  
Species Production

The Catalytically Active Copper-Amyloid-Beta State: Coordination Site Responsible for Reactive Oxygen Species Production

2013 ◽  
Vol 52 (42) ◽  
pp. 11110-11113 ◽  
Author(s):  
Laure-Estelle Cassagnes ◽  
Vincent Hervé ◽  
Françoise Nepveu ◽  
Christelle Hureau ◽  
Peter Faller ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Amyloid Beta ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Coordination Site ◽  
Catalytically Active ◽  
State Coordination ◽  
Species Production

scholarly journals New Insights in the Amyloid-Beta Interaction with Mitochondria

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Carlos Spuch ◽  
Saida Ortolano ◽  
Carmen Navarro
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Mitochondrial Dysfunction ◽  
Amyloid Beta ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Mitochondrial Proteins ◽  
Oxygen Species ◽  
Species Production

Biochemical and morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer’s disease (AD). Particularly, mitochondrial dysfunction is a hallmark of amyloid-beta-induced neuronal toxicity in Alzheimer’s disease. The recent emphasis on the intracellular biology of amyloid-beta and its precursor protein (APP) has led researchers to consider the possibility that mitochondria-associated and mitochondrial amyloid-beta may directly cause neurotoxicity. Both proteins are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron transport chain, increase reactive oxygen species production, cause mitochondrial damage, and prevent neurons from functioning normally. In this paper, we will outline current knowledge of the intracellular localization of amyloid-beta. Moreover, we summarize evidence from AD postmortem brain as well as animal AD models showing that amyloid-beta triggers mitochondrial dysfunction through a number of pathways such as impairment of oxidative phosphorylation, elevation of reactive oxygen species production, alteration of mitochondrial dynamics, and interaction with mitochondrial proteins. Thus, this paper supports the Alzheimer cascade mitochondrial hypothesis such as the most important early events in this disease, and probably one of the future strategies on the therapy of this neurodegenerative disease.

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