A neurotoxic peptide β-amyloid (Aβ) is linked to the beginning of Alzheimer’s disease (AD). The accumulation of amyloid-beta inside mitochondria boosts production of free radical and activation of the apoptotic pathway. Human Presequence Protease (hPreP, PITRM1) is a mitochondrial ATP-independent metalloprotease. It degrades toxic peptides, including mitochondrial presequences and β-amyloid. This enzyme is an attractive target for Alzheimer’s disease drug design because enhancement of it's activity increases the level of Aβ proteolysis.

Glucocorticoids (GCs) are secreted from the adrenal gland in response to exposure to emotional and physiologic stressors and are responsible for modulating essential metabolic, cardiovascular, immune, and behavioral functions [1–3]. The glucocorticoid receptor (GR) belongs to a family of nuclear hormone receptors that are ligand-dependent transcription factors.