A Synergistic Dysfunction of Mitochondrial Fission/Fusion Dynamics and Mitophagy in Alzheimer's Disease

Renato X. Santos, Sonia 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

141 Citations (Scopus)


Alzheimer's disease (AD), the most common form of dementia in the elderly, can have a late-onset sporadic or an early-onset familial origin. In both cases, the neuropathological hallmarks are the same: senile plaques and neurofibrillary tangles. Despite AD having a proteinopathic nature, there is strong evidence for an organelle dysfunction-related neuropathology, namely dysfunctional mitochondria. In this regard, dysfunctional mitochondria and associated exacerbated generation of reactive oxygen species are among the earliest events in the progression of the disease. Since the maintenance of a healthy mitochondrial pool is essential given the central role of this organelle in several determinant cellular processes, mitochondrial dysfunction in AD would be predicted to have profound pluripotent deleterious consequences. Mechanistically, recent reports suggest that mitochondrial fission/fusion and mitophagy are altered in AD and in in vitro models of disease, and since both processes are reported to be protective, this review will discuss the role of mitochondrial fission/fusion and mitophagy in the pathogenesis of AD.
Original languageEnglish
Pages (from-to)S401-S412
Number of pages12
JournalJournal of Alzheimer's Disease
Issue numbers2
Publication statusPublished - 3 Jun 2010

Bibliographical note

Work in the authors’ laboratories is supported by the National Institutes of Health (AG024028 and AG031852) and the Alzheimer’s Association.
Authors’ disclosures available online (http://www.jalz.com/disclosures/view.php?id=445).


  • Alzheimer's disease
  • fission
  • fusion
  • mitochondrial dysfunction
  • mitophagy


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