Effects of stress and stress hormones on amyloid-beta protein and plaque deposition.
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-beta protein, and amyloid-beta 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.
Dong
Hongxin
H
Department of Psychiatry and Behavioral Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. h-dong@northwestern.edu
Csernansky
John G
JG
D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008822:Mice, Transgenic; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism; D058225:Plaque, Amyloid / Q000378:metabolism*; D012934:Social Isolation / Q000523:psychology; D013315:Stress, Psychological / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
D016229:Amyloid beta-Peptides; D006728:Hormones; D003346:Corticotropin-Releasing Hormone