This study is consistent with the body of literature associating Abeta oligomers with increased calcium entry through glutamate receptors, and nicely traces the mechanistic path from receptor activation to apoptosis.

Although the results clearly indicate that Abeta is triggering calcium dysregulation, this study also contains many of the technical concerns seen throughout this body of literature...such as supraphysiological concentrations of Abeta, acute bolus applications, and the use of embryonic or peri-natal cultured neurons (whose glutamatergic receptor population differs from a mature or aged animal). These conditions do not necessarily negate the findings, but do require some qualifications or restrictions when extrapolating to late-stage, slowly developing, degenerative diseases.

View all comments by Grace (Beth) Stutzmann