Calcium homeostasis is dysregulated in AD, but there is debate about whether this is a cause or consequence of neuronal dysfunction, and concerning how amyloid pathology causes neuronal calcium dyshomeostasis. We observe that high concentrations of Aß42 elevate calcium in primary neurons and in dystrophic neurites around plaques, and preliminary data indicate that the calcium release-activated calcium (CRAC) channels may play a role. We will validate the role of CRAC channels in Aß42-induced caclium elevation in neurons, AD mouse models and AD brain tissues to determine the potential of CRAC channels as a novel therapeutic target in AD.
|Effective start/end date||7/1/15 → 6/30/16|
- Illinois Department of Public Health (63282001D)
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