Publications by authors named "C Waites"

Article Synopsis
  • Chronic stress and elevated glucocorticoids increase the risk and accelerate the progression of Alzheimer's disease (AD) by influencing the disease's key features, like tau tangles and amyloid plaques.
  • Research indicates that stress hormones disrupt vital cellular processes, including protein management and energy production, which are crucial in AD development.
  • The review covers findings from animal and cellular studies that demonstrate how chronic stress and glucocorticoids affect tau and amyloid pathology, inflammation, and barrier functions in the brain.
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Chronic stress and elevated levels of glucocorticoids (GCs), the main stress hormones, accelerate Alzheimer's disease (AD) onset and progression. A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. While stress and high GC levels are known to induce intraneuronal Tau pathology (i.

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Chronic stress and elevated levels of glucocorticoids (GCs), the main stress hormones, accelerate Alzheimer's disease (AD) onset and progression. A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. While stress and high GC levels are known to induce intraneuronal Tau pathology (.

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Chronic stress and elevated levels of glucocorticoids (GCs), the main stress hormones, accelerate Alzheimer's disease (AD) onset and progression. A major driver of AD progression is the spreading of pathogenic Tau protein between brain regions, precipitated by neuronal Tau secretion. While stress and high GC levels are known to induce intraneuronal Tau pathology ( hyperphosphorylation, oligomerization) in animal models, their role in trans-neuronal Tau spreading is unexplored.

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Prolonged exposure to glucocorticoids, the main stress hormones, damages the brain and is a risk factor for depression and Alzheimer's disease. Two major drivers of glucocorticoid-related neurotoxicity are mitochondrial dysfunction and Tau pathology; however, the molecular/cellular mechanisms precipitating these events, and their causal relationship, remain unclear. Using cultured murine hippocampal neurons and 4-5-month-old mice treated with the synthetic glucocorticoid dexamethasone, we investigate the mechanisms underlying glucocorticoid-induced mitochondrial damage and Tau pathology.

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