The Role of Elevated Glucocorticoid Levels in Alzheimer’s Disease Pathologies
DOI:
https://doi.org/10.58445/rars.1693Keywords:
Alzheimer’s disease, glucocorticoids, cortisol, hypothalamus-pituitary-adrenal axis, memory impairmentAbstract
Alzheimer’s disease (AD), the most common type of dementia, is a neurodegenerative disease related to the loss of memory and cognitive functions. Due to the fact that there has been no cure discovered for Alzheimer’s disease, researchers have been trying to investigate AD pathologies to reduce the risks and symptoms. Emerging evidence suggests that chronic stress, which leads to elevated levels of glucocorticoids (GC), is thought to be one of the critical factors to the development and progression of Alzheimer’s disease. Chronic exposure of glucocorticoids to the brain creates neurotoxic effects, which is thought to impair the brain and contribute to the development of AD. Furthermore, glucocorticoids exacerbate the brain damage caused by AD, such as cerebral atrophy, amyloid-β production, and tau hyperphosphorylation. This review focuses on recent studies over the relationships between elevated levels of glucocorticoids and Alzheimer’s disease pathology, such as amyloid-β peptide plaques and tau tangles, neuroinflammation, the cortisol awakening response, and cerebral structures. Elevated levels of glucocorticoids have been shown to have a significant role in the progression of AD. Exploring this relationship can help answer the complexities of this disease. With further research over this correlation, intervention methods to prevent or delay the development of AD may be discovered, potentially through decreasing high glucocorticoid levels.
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