Alzheimer's disease: diverse aspects of mitochondrial malfunctioning

Renato X. Santos, Sónia C. Correia, Xinglong Wang, George Perry, Mark A. Smith, Paula I. Moreira, Xiongwei Zhu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

107 Citations (Scopus)


Alzheimer’s disease is a progressive neurodegenerative disorder, either assuming a sporadic, age-associated, late-onset form, or a familial form, with early onset, in a smaller fraction of the cases. Whereas in the familial cases several mutations have been identified in genes encoding proteins related with the pathogenesis of the disease, for the sporadic form several causes have been proposed and are currently under debate. Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of Alzheimer’s disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to its onset and progression. (IJCEP1006004).
Original languageEnglish
Pages (from-to)570-581
Number of pages12
JournalInternational journal of clinical and experimental pathology
Issue number6
Early online date25 Jun 2010
Publication statusPublished - Jun 2010
Externally publishedYes

Bibliographical note

This study is supported by the NIH (AG031852) and Alzheimer’s Association (IIRG-07-60196).


  • Alzheimer’s disease
  • mitochondria
  • mitochondrial dysfunction
  • mitochondrial dynamics


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