Hayley M, Perspicace S, Schulthess T, Seelig J.
Calcium enhances the proteolytic activity of BACE1: An in vitro biophysical and biochemical characterization of the BACE1-calcium interaction.
Biochim Biophys Acta. 2009 Sep;1788(9):1933-8.
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This is an enlightening study that expands upon the role of calcium signaling in AD pathogenesis. One word of caution/clarification is that in neurons, micromolar calcium concentrations are actually high and are maintained only transiently (resting levels are in the nanomolar range). These higher concentrations can be achieved in localized regions during high synaptic activity, calcium release from ER stores (known to be increased with PS mutations), and metabolic stress. Possibly then, AD mutations or neuronal activity that leads to more sustained increases in calcium levels may feed into upregulated BACE1 activity and increased Abeta production.