Amyloid-Beta interaction with mitochondria

Pagani, Lucia and Eckert, Anne. (2011) Amyloid-Beta interaction with mitochondria. International journal of Alzheimer's disease, Vol. 2011 , 925050.

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Official URL: http://edoc.unibas.ch/dok/A6004730

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Mitochondrial dysfunction is a hallmark of amyloid-beta(A?)-induced neuronal toxicity in Alzheimer's disease (AD). The recent emphasis on the intracellular biology of A? and its precursor protein (A?PP) has led researchers to consider the possibility that mitochondria-associated and/or intramitochondrial A? may directly cause neurotoxicity. In this paper, we will outline current knowledge of the intracellular localization of both A? and A?PP addressing the question of how A? can access mitochondria. Moreover, we summarize evidence from AD postmortem brain as well as cellular and animal AD models showing that A? triggers mitochondrial dysfunction through a number of pathways such as impairment of oxidative phosphorylation, elevation of reactive oxygen species (ROS) production, alteration of mitochondrial dynamics, and interaction with mitochondrial proteins. In particular, we focus on A? interaction with different mitochondrial targets including the outer mitochondrial membrane, intermembrane space, inner mitochondrial membrane, and the matrix. Thus, this paper establishes a modified model of the Alzheimer cascade mitochondrial hypothesis.
Faculties and Departments:03 Faculty of Medicine > Bereich Psychiatrie (Klinik) > Erwachsenenpsychiatrie UPK > Erwachsenenpsychiatrie (Lang)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Psychiatrie (Klinik) > Erwachsenenpsychiatrie UPK > Erwachsenenpsychiatrie (Lang)
UniBasel Contributors:Eckert, Anne
Item Type:Article, refereed
Article Subtype:Research Article
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:25 Oct 2013 08:32
Deposited On:25 Oct 2013 08:32

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