Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep33781
Keywords
-
Categories
Funding
- Ministry of Education Singapore [R-184-000-230-112, 2014-T2-2-120]
- Yale-NUS start-up grant
- NUS Graduate School for Integrative Sciences and Engineering
Ask authors/readers for more resources
Alzheimer Disease (AD) is a progressive neurological disorder characterized by the deposition of amyloid beta (A beta), predominantly the A beta(1-42) form, in the brain. Mitochondrial dysfunction and impaired energy metabolism are important components of AD pathogenesis. However, the causal and temporal relationships between them and AD pathology remain unclear. Using a novel C. elegans AD strain with constitutive neuronal A beta(1-42) expression that displays neuromuscular defects and age-dependent behavioural dysfunction reminiscent of AD, we have shown that mitochondrial bioenergetic deficit is an early event in AD pathogenesis, preceding dysfunction of mitochondrial electron transfer chain (ETC) complexes and the onset of global metabolic failure. These results are consistent with an emerging view that AD may be a metabolic neurodegenerative disease, and also confirm that A beta-driven metabolic and mitochondrial effects can be reproduced in organisms separated by large evolutionary distances.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available