. Mitochondrial Ca2+ overload underlies Abeta oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs. PLoS One. 2008;3(7):e2718. PubMed.


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  1. This paper describes how amyloid-β oligomers promote calcium influx, and how excessive mitochondrial Ca2+ damages the structure and function of mitochondria of Alzheimer disease neurons. The outcome of this paper may improve our basic understanding of amyloid-β oligomer toxicity, Ca2+ influx, and mitochondrial dysfunction, and may have implications for mitochondrial and calcium therapeutics for Alzheimer disease.

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