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Abstract: The effects of β amyloid (Aβ) on cytoplasmic Ca2+ ([Ca2+]c) have been studied extensively, but the current literature on this aspect is confusing. We reported that 20μM Aβ25–35 significantly inhibited the synchronized spontaneous cytoplasmic Ca2+ transients immediately after application, whereas it had little effect on the baseline [Ca2+]c concentration in neurons. Aβ1–42 had a similar effect on the Ca2+ transients as Aβ25–35, while it increased baseline [Ca2+]c concentration gradually. However, Aβ1–40 had little effect on either Ca2+ transients or baseline [Ca2+]c. Such differential effects of Aβ on Ca2+ signals might explain, at least partially, the confusing observations from the previous studies and provide important therapeutic implications for preventing or reversing early neuron damage in Alzheimer''s disease. [Copyright &y& Elsevier]

The effects of beta amyloid (Abeta) on cytoplasmic Ca(2+) ([Ca(2+)](c)) have been studied extensively, but the current literature on this aspect is confusing. We reported that 20 microM Abeta(25-35) significantly inhibited the synchronized spontaneous cytoplasmic Ca(2+) transients immediately after application, whereas it had little effect on the baseline [Ca(2+)](c) concentration in neurons. Abeta(1-42) had a similar effect on the Ca(2+) transients as Abeta(25-35), while it increased baseline [Ca(2+)](c) concentration gradually. However, Abeta(1-40) had little effect on either Ca(2+) transients or baseline [Ca(2+)](c). Such differential effects of Abeta on Ca(2+) signals might explain, at least partially, the confusing observations from the previous studies and provide important therapeutic implications for preventing or reversing early neuron damage in Alzheimer's disease.