ORAI2 Down-Regulation Potentiates SOCE and Decreases Aβ42 Accumulation in Human Neuroglioma Cells.

ABSTRACT: Senile plaques, the hallmarks of Alzheimer's Disease (AD), are generated by the deposition of amyloid-beta (Aβ), the proteolytic product of amyloid precursor protein (APP), by β and γ-secretase. A large body of evidence points towards a role for Ca²⁺ imbalances in the pathophysiology of both sporadic and familial forms of AD (FAD). A reduction in store-operated Ca²⁺ entry (SOCE) is shared by numerous FAD-linked mutations, and SOCE is involved in Aβ accumulation in different model cells. In neurons, both the role and components of SOCE remain quite obscure, whereas in astrocytes, SOCE controls their Ca²⁺-based excitability and communication to neurons. Glial cells are also directly involved in Aβ production and clearance. Here, we focus on the role of ORAI2,

SUBMITTER: Scremin E 

PROVIDER: S-EPMC7432374 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature