Affiliations: Department of Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA | Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA
Correspondence:
[*]
Corresponding author: Hongxin Dong, MD PhD, Department of Psychiatry and Behavior Sciences, Feinberg School of Medicine, Northwestern University, Ward 9-198, 303 E. Chicago Avenue, Chicago, IL 60611, USA. Tel.: +1 312 503 3433; Fax: +1 312 503 0466; E-mail: h-dong@northwestern.edu.
Abstract: Growing evidence indicates that physical and psychosocial stressors, in part acting through the hypothalamic-pituitary-adrenal (HPA) axis, may accelerate the process of Alzheimer's disease (AD). In this review, we summarize recent research related to the effects of stress and stress hormones on the various disease process elements associated with AD. Specifically, we focus on the relationships among chronic stressors, HPA axis activity, amyloid-β protein, and amyloid-β plaque deposition in mouse models of AD. The potential mechanisms by which stress and stress-related components, especially corticotrophin-releasing factor and its receptors, influence the pathogenesis of AD are discussed.
