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-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.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Amyloid beta-Peptides / metabolism*
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Animals
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Brain / metabolism
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Brain / pathology
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Corticotropin-Releasing Hormone / pharmacology
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Hormones / metabolism*
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Humans
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Hypothalamo-Hypophyseal System / drug effects
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Hypothalamo-Hypophyseal System / metabolism
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Mice
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Mice, Transgenic
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Neurons / drug effects
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Neurons / pathology
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Pituitary-Adrenal System / drug effects
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Pituitary-Adrenal System / metabolism
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Plaque, Amyloid / metabolism*
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Social Isolation / psychology
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Stress, Psychological* / metabolism
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Stress, Psychological* / pathology
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Stress, Psychological* / physiopathology
Substances
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Amyloid beta-Peptides
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Hormones
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Corticotropin-Releasing Hormone