Journal
NEURODEGENERATIVE DISEASES
Volume 7, Issue 1-3, Pages 56-59Publisher
KARGER
DOI: 10.1159/000283484
Keywords
A beta-derived diffusible ligands; Mitochondria; Axonal transport; Alzheimer's disease
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Funding
- NIH [AG 031852]
- Alzheimer's Association [IIRG-07-60196, Zen-07-59500]
- Memory and Cognition Center at Case Western Reserve University
- NATIONAL INSTITUTE ON AGING [R01AG031852] Funding Source: NIH RePORTER
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Background: Alzheimer's disease (AD) is the most prevalent form of dementia predominantly affecting the elderly. It is believed that soluble amyloid-beta (A beta) oligomers are involved in the pathogenesis of AD, yet the underlying mechanisms remain elusive. Objectives: Emerging evidence suggests that mitochondrial dysfunction likely plays a critical role in A beta-induced neuronal degeneration. Previously, we demonstrated that A beta-derived diffusible ligands (ADDLs) induce reduced mitochondrial density in neurites, and we suspect that an impaired mitochondrial trafficking might be involved, which is tested in this study. Methods: Using live cell imaging, anterograde and retrograde transport of mitochondria in primary hippocampal neurons treated with sublethal doses of ADDLs was measured. Results: We found that ADDLs induced significant impairment in both anterograde and retrograde transport of mitochondria along axons. Conclusion: These results suggest that an impaired mitochondrial transport likely contributes to ADDL-induced abnormal mitochondrial distribution and dysfunction and also reinforce the idea that axonal transport is likely involved in AD pathogenesis. Copyright (C) 2010 S. Karger AG, Basel
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