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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 780179, 11 pages
Review Article

Mitochondrial Dysfunction: Different Routes to Alzheimer’s Disease Therapy

Istituto di Biomedicina ed Immunologia Molecolare (IBIM) “Alberto Monroy,” CNR, via Ugo La Malfa 153, 90146 Palermo, Italy

Received 19 March 2014; Accepted 29 May 2014; Published 20 August 2014

Academic Editor: Giles E. Hardingham

Copyright © 2014 Pasquale Picone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondria are dynamic ATP-generating organelle which contribute to many cellular functions including bioenergetics processes, intracellular calcium regulation, alteration of reduction-oxidation potential of cells, free radical scavenging, and activation of caspase mediated cell death. Mitochondrial functions can be negatively affected by amyloid β peptide (Aβ), an important component in Alzheimer’s disease (AD) pathogenesis, and Aβ can interact with mitochondria and cause mitochondrial dysfunction. One of the most accepted hypotheses for AD onset implicates that mitochondrial dysfunction and oxidative stress are one of the primary events in the insurgence of the pathology. Here, we examine structural and functional mitochondrial changes in presence of Aβ. In particular we review data concerning Aβ import into mitochondrion and its involvement in mitochondrial oxidative stress, bioenergetics, biogenesis, trafficking, mitochondrial permeability transition pore (mPTP) formation, and mitochondrial protein interaction. Moreover, the development of AD therapy targeting mitochondria is also discussed.