Affiliations: [a] Center for Neuroscience and Cell Biology, Institute of Physiology – Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal | [b] Center for Neuroscience and Cell Biology, Institute of Biochemistry – Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal | [c] Center for Neuroscience and Cell Biology, Department of Zoology – Faculty of Sciences and Technology, University of Coimbra, 3004-504 Coimbra, Portugal | [x] Center for Neuroscience and Cell Biology, Institute of Physiology – Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal | [y] Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Correspondence:
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Corresponding author: C.R. Oliveira, Center for Neurosciences and Cell Biology and Institute of Biochemistry, Faculty of Medicine, University of Coimbra, 3004-504 Coimbra, Portugal. Tel.: +351 239 820190; Fax: +351 239 822776; E-mail: catarina@cnc.cj.uc.pt.
Note: [1] The authors contributed equally to this review.
Abstract: Mitochondria are uniquely poised to play a pivotal role in neuronal cell survival or death because they are regulators of both energy metabolism and apoptotic pathways. This review is mainly focused in the discussion of evidence suggesting a clear association between amyloid-β toxicity, mitochondrial dysfunction, oxidative stress and neuronal damage/death in Alzheimer's disease pathophysiology. The knowledge that mitochondrial dysfunction has a preponderant role in Alzheimer's disease opened a window for new therapeutic strategies aimed to preserve/ameliorate mitochondrial function. Based on recent developments in mitochondrial research, increased pharmacological and pharmaceutical efforts have lead to the emergence of 'Mitochondrial Medicine' as a whole new field of biomedical research being this topic discussed in the last section of this review.
