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pubmed:abstractText |
The cellular mechanism by which beta-amyloid has its effect on neurons is unknown. Based on observations that endogenous neurotoxins, such as glutamate and platelet activating factor (PAF), cause activation of cytoplasmic calcium, we tested if this was true with beta-amyloid. Using nerve growth factor-treated PC12 cells, we noted that the active beta-amyloid fragment, containing residues 25 to 35, caused a specific and dose-dependent increase in intracellular calcium due to an influx of extracellular calcium.
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