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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Texas Tech University Health Sciences Center
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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