Although the precise culprit in the etiopathogenesis of Alzheimer disease (AD) is still obscure, defective mitochondria functioning has been proposed to be an upstream event in AD. Mitochondria fulfill a number of essential cellular functions, and it is recognized that the strict regulation of the structure, function and turnover of these organelles is an immutable control node for the maintenance of neuronal and vascular homeostasis. Extensive research in postmortem brain tissue from AD subjects, and AD animal and cellular models revealed that mitochondria undergo multiple malfunctions during the course of this disease. The present review summarizes the current views on how mitochondria are implicated in both AD-related neuronal and cerebrovascular degeneration. The understanding of the mitochondrial mechanisms underlying AD pathology is critical to design more effective strategies to halt or delay disease progression.
Bibliographical noteCopyright © 2012 Elsevier Inc. All rights reserved.
Acknowledgements The authors’work is supported by the Fundação para a Ciência e a Tecnologia co-funded by Fundo Europeu para o Desenvolvimento Regional (PTDC/SAU-NEU/103325/2008 and PTDC/SAU-NMC/110990/2009) via Programa Operacional Factores de Competitividade, and Quadro de Referência Estratégico Nacional (QREN DO-IT). Sónia C. Correia has a PhD fellowship from the Fundação para a Ciência e a Tecnologia (SFRH/BD/40702/2007)
- Alzheimer Disease/physiopathology
- Cerebrovascular Disorders/physiopathology
- Disease Models, Animal
- Disease Progression
- Mitochondrial Diseases/physiopathology