Abstract
Alzheimer's disease (AD) is a relentless neurodegenerative disease affecting more than 36 million people worldwide. Increased evidence suggests stress and its synonymous elevated circulating glucocorticoid levels, due to dysregulation of Hypothalamic-Pituitary-Adrenal (HPA) axis, is an important environmental risk factor for the onset and progression of AD [1]. Here we review recent data on the effect of glucocorticoids on spontaneous activity of HPA axis with particular emphasis on AD, and how modulation of glucocorticoid (GC) levels or GC receptors (GCRs) could potentially mediate disease processes. Early phase of AD is characterized by hippocampal memory (episodic memory) loss and impaired synaptic plasticity [2]. In a study at IPMC in France on mouse model AD, treatment with GCR antagonist, mifepristone (RU486) reduced cerebral B Amyloid (AB), Tau pathologies and cognitive impairment [3]. Pointing to a potential therapeutic role for interventions to underlying HPA axis and GCRs activity.
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