A reciprocal relationship between reactive oxygen species and mitochondrial dynamics in neurodegeneration

Clara Hiu Ling Hung, Sally Shuk Yee Cheng, Yuen Ting Cheung, Suthicha Wuwongse, Natalie Qishan Zhang, Yuen Shan Ho, Simon Ming Yuen Lee, Raymond Chuen Chung Chang

Research output: Journal article publicationJournal articleAcademic researchpeer-review

94 Citations (Scopus)


Mitochondrial fragmentation due to fission/fusion imbalance has often been linked to mitochondrial dysfunction and apoptosis in neurodegeneration. Conventionally, it is believed that once mitochondrial morphology shifts away from its physiological tubular form, mitochondria become defective and downstream apoptotic signaling pathways are triggered. However, our study shows that beta-amyloid (Aβ) induces morphological changes in mitochondria where they become granular-shaped and are distinct from fragmented mitochondria in terms of both morphology and functions. Accumulation of mitochondrial reactive oxygen species triggers granular mitochondria formation, while mitoTEMPO (a mitochondria-targeted superoxide scavenger) restores tubular mitochondrial morphology within Aβ-treated neurons. Interestingly, modulations of mitochondria fission and fusion by genetic and pharmacological tools attenuated not only the induction of granular mitochondria, but also mitochondrial superoxide levels in Aβ−treated neurons. Our study shows a reciprocal relationship between mitochondrial dynamics and reactive oxygen species and provides a new potential therapeutic target at early stages of neurodegenerative disease pathogenesis.

Original languageEnglish
Pages (from-to)7-19
Number of pages13
JournalRedox Biology
Publication statusPublished - Apr 2018


  • Alzheimer's disease
  • Drp-1
  • Fission and fusion
  • Mitochondria
  • Neurodegeneration
  • β-amyloid

ASJC Scopus subject areas

  • Organic Chemistry
  • Clinical Biochemistry


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