Journal
PLOS ONE
Volume 7, Issue 11, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0048225
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Funding
- Alzheimer's Research UK
- Alzheimer's Brain Bank UK
- BRACE (Bristol Research into Alzheimer's and Care of the Elderly)
- BBSRC CASE PhD studentship
- Eli Lilly Co. Ltd
- Lister Institute for Preventive Medicine Prize Fellowship
- Alzheimers Research UK [ART-EG2005B-1] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/E500110/1] Funding Source: researchfish
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Progressive mitochondrial dysfunction contributes to neuronal degeneration in age-mediated disease. An essential regulator of mitochondrial function is the deacetylase, sirtuin 3 (SIRT3). Here we investigate a role for CNS Sirt3 in mitochondrial responses to reactive oxygen species (ROS)- and Alzheimer's disease (AD)-mediated stress. Pharmacological augmentation of mitochondrial ROS increases Sirt3 expression in primary hippocampal culture with SIRT3 over-expression being neuroprotective. Furthermore, Sirt3 expression mirrors spatiotemporal deposition of beta-amyloid in an AD mouse model and is also upregulated in AD patient temporal neocortex. Thus, our data suggest a role for SIRT3 in mechanisms sensing and tackling ROS- and AD-mediated mitochondrial stress.
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