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
Summary
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).
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