Introduction: Alzheimer's disease (AD) is linked to neuronal calcium dyshomeostasis, which is associated with network hyperexcitability. Decreased expression of the calcium-binding protein cal- bindin-D (CB) might be a susceptibility factor for AD. The subiculum is affected early in AD, for unknown reasons.
Methods: In AD, CB knock-out and control mice fluorescence Ca imaging combined with patch clamp were used to characterize Ca dynamics, resting Ca , and Ca -buffering capacity in subicular neurons. CB expression levels in wild-type and AD mice were also analyzed.
Results: The subiculum and dentate gyrus of wild-type mice showed age-related decline in CB expression not observed in AD mice. Resting Ca and Ca -buffering capacity was increased in aged AD mice subicular dendrites. Modeling suggests that AD calcium changes can be explained by alterations of Ca extrusion pumps rather than by buffers.
Discussion: Overall, abnormal Ca homeostasis in AD has an age dependency that comprises multiple mechanisms, including compensatory processes.
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