Amyloid pathology‐produced unexpected modifications of calcium homeostasis in hippocampal subicular dendrites. Issue 2 (6th January 2020)

• Record Type: Journal Article
• Authors: Angulo, Sergio L.; Henzi, Thomas; Neymotin, Samuel A.; Suarez, Manuel D.; Lytton, William W.; Schwaller, Beat; Moreno, Herman
• Is Part Of: Alzheimer's & dementia. Volume 16:Issue 2(2020)
• Page Start: 251
• Page End: 261
• Publication Date: 2020-01-06
• Subjects: Alzheimer's disease -- Calbindin -- Calcium homeostasis -- Calcium imaging -- Patch clamp -- Subiculum; Alzheimer's disease -- Periodicals; Alzheimer Disease -- Periodicals; Dementia -- Periodicals; Démence; Maladie d'Alzheimer; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.83
• DOI: 10.1016/j.jalz.2019.07.017
• Languages: English
• ISSNs: 1552-5260

Abstract

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 Ca 2+ imaging combined with patch clamp were used to characterize Ca 2+ dynamics, resting Ca 2+, and Ca 2+ ‐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 2+ and Ca 2+ ‐buffering capacity was increased in aged AD mice subicular dendrites. Modeling suggests that AD calcium changes can be explained by alterations of Ca 2+ extrusion pumps rather than by buffers. Discussion: Overall, abnormal Ca 2+ homeostasis in AD has an age dependency that comprises multiple mechanisms, including compensatory processes.