Mitochondrial Ca2+ overload underlies Abeta oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs.
Dysregulation of intracellular Ca(2+) homeostasis may underlie amyloid beta peptide (Abeta) toxicity in Alzheimer's Disease (AD) but the mechanism is unknown. In search for this mechanism we found that Abeta(1-42) oligomers, the assembly state correlating best with cognitive decline in AD, but...
Main Authors: | , , , , |
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Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2008-01-01
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Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC2447871?pdf=render |