Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/74592
Title: A reciprocal relationship between reactive oxygen species and mitochondrial dynamics in neurodegeneration
Authors: Hung, CHL
Cheng, SSY
Cheung, YT
Wuwongse, S
Zhang, NQ
Ho, YS 
Lee, SMY
Chang, RCC
Keywords: Alzheimer's disease
Drp-1
Fission and fusion
Mitochondria
Neurodegeneration
β-amyloid
Issue Date: 2018
Publisher: Chinese Chemical Society
Source: Redox biology, 2018, v. 14, p. 7-19 How to cite?
Journal: Redox biology 
Abstract: 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.
URI: http://hdl.handle.net/10397/74592
ISSN: 2213-2317
DOI: 10.1016/j.redox.2017.08.010
Rights: © 2017 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/).
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