Customer Publication

Chronic glucocorticoid exposure accelerates Aβ generation and neurotoxicity by activating calcium-mediated CN-NFAT1 signaling in hippocampal neurons in APP/PS1 mice

Authors: Ding et al.

Journal: Food and Chemical Toxicology (2022)

Institution: Anhui Medical University

Research Areas: Alzheimer’s disease

Cell Lines: Primary hippocampal neurons

Summary: Glucocorticoid (GC) exposure can lead to deterioration of the structure and function of hippocampal neurons and is closely involved in Alzheimer’s disease (AD). Amyloid-β (Aβ) overproduction is an important aspect of AD pathogenesis. The study mainly investigated the mechanism of chronic GC exposure in accelerating Aβ production in primary cultured hippocampal neurons from APP/PS1 mice. This study indicates that chronic DEX exposure accelerates Aβ accumulation by activating calcium-mediated CN-NFAT1 signaling in hippocampal neurons from APP/PS1 mice, which may be closely related to the acceleration of AD. HoloMonitor M4 was used to study the effect of chronic DEX exposure on cell viability by measuring different morphological characteristics and cell motility.

Keywords: HoloMonitor M4, cell morphology, cell motility, Alzheimer's diseases, Glucocorticoids, Calcium homeostasis disorder, Nuclear factor of activated T cells 1 (NFAT1), Aβ generation

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