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. 2020 Feb;16(2):251-261.
doi: 10.1016/j.jalz.2019.07.017. Epub 2020 Jan 6.

Amyloid pathology-produced unexpected modifications of calcium homeostasis in hippocampal subicular dendrites

Sergio L Angulo  1 , Thomas Henzi  2 , Samuel A Neymotin  3 , Manuel D Suarez  1 , William W Lytton  1   4 , Beat Schwaller  2 , Herman Moreno  1   4
Affiliations

Amyloid pathology-produced unexpected modifications of calcium homeostasis in hippocampal subicular dendrites

Sergio L Angulo et al. Alzheimers Dement. 2020 Feb.

Abstract

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-D28K (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 Ca2+ imaging combined with patch clamp were used to characterize Ca2+ dynamics, resting Ca2+ , and Ca2+ -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 Ca2+ and Ca2+ -buffering capacity was increased in aged AD mice subicular dendrites. Modeling suggests that AD calcium changes can be explained by alterations of Ca2+ extrusion pumps rather than by buffers.

Discussion: Overall, abnormal Ca2+ homeostasis in AD has an age dependency that comprises multiple mechanisms, including compensatory processes.

Keywords: Alzheimer's disease; Calbindin; Calcium homeostasis; Calcium imaging; Patch clamp; Subiculum.

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References

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