Abstract
Memory loss is the most prominent clinical aspect of Alzheimer’s disease (AD) but, as recent clinical evidence has been revealed, intervening when memory difficulties are already apparent does little to alter the morbidity and mortality of the disease. Therefore, risk factors that accelerate the development of AD have recently received tremendous interest. Among those risk factors, interrogation of stress hormones/glucocorticoids have been particularly impactful because stress is an inherent aspect of life and unavoidable. Heightened indices of stress in mid-life predict greater risk for AD in late-life, stress hormone dysregulation in the aged increases AD vulnerability and higher levels of circulating glucocorticoid in AD patients correlates with faster cognitive decline. However, despite this evidence, the precise mechanism linking glucocorticoids and stress hormone to AD remain elusive.
In this chapter, we provide an overview of the hypothalamus–pituitary–adrenal (HPA) axis, and how stress, dysregulation of stress hormones and HPA axis dysfunction are currently thought to play a role in AD pathogenesis.
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Joshi, Y.B., Praticò, D. (2013). Stress and HPA Axis Dysfunction in Alzheimer’s Disease. In: Praticὸ, D., Mecocci, P. (eds) Studies on Alzheimer's Disease. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-62703-598-9_11
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DOI: https://doi.org/10.1007/978-1-62703-598-9_11
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