Abstract

Amyloid β-peptide oligomers, ryanodine receptor-mediated Ca2+ release, and Wnt-5a/Ca2+ signaling: opposing roles in neuronal mitochondrial dynamics?

Highlights

  • Alzheimer’s disease (AD) is the most common form of dementia in the elderly (Querfurth and Laferla, 2010)

  • We have reported that the long-lasting Ca2+ signals generated by Aβ oligomers (AβOs) in primary hippocampal neurons disrupt mitochondrial network structure; suppressing ryanodine receptor (RyR) activity by pre-incubation with inhibitory ryanodine prevents AβOs-induced mitochondrial fission, indicating that this process requires the RyR-mediated Ca2+ signals generated by AβOs (Paula-Lima et al, 2011)

  • The work by Silva-Alvarez and colleagues confirms that RyR inhibition with ryanodine prevents the alterations in mitochondrial morphology induced by AβOs

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Summary

Introduction

Alzheimer’s disease (AD) is the most common form of dementia in the elderly (Querfurth and Laferla, 2010). We have reported that the long-lasting Ca2+ signals generated by AβOs in primary hippocampal neurons disrupt mitochondrial network structure; suppressing RyR activity by pre-incubation with inhibitory ryanodine prevents AβOs-induced mitochondrial fission, indicating that this process requires the RyR-mediated Ca2+ signals generated by AβOs (Paula-Lima et al, 2011).

Results
Conclusion

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