Amyloid-β-derived diffusible ligands cause impaired axonal transport of mitochondria in neurons

Xinglong Wang, George Perry, Mark A. Smith, Xiongwei Zhu

Research output: Contribution to journalArticlepeer-review

Abstract

Background: Alzheimer's disease (AD) is the most prevalent form of dementia predominantly affecting the elderly. It is believed that soluble amyloid-β (Aβ) 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 Aβ-induced neuronal degeneration. Previously, we demonstrated that Aβ-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 sub-lethal 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.

Original languageEnglish (US)
Pages (from-to)56-59
Number of pages4
JournalNeurodegenerative Diseases
Volume7
Issue number1-3
DOIs
StatePublished - Apr 2010
Externally publishedYes

Keywords

  • Aβ-derived diffusible ligands
  • Alzheimer's disease
  • Axonal transport
  • Mitochondria

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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