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Mechanistic Links Between Chronic Stress and Alzheimer’s Disease:HPA Axis Activation and Neuroinflammation
Abstract
Alzheimer’s Disease (AD) pathology has been shown to begin decades before theappearance of cognitive symptoms. This is backed by imaging and biomarker studies showing amyloid and tau abnormalities followed by neurodegeneration (Ottoy et al., 2025). Hence, current research being done to understand the cause of Alzheimer’s focuses on the “plaques and tangles” theory, in which amyloid beta (Aβ) deposits build up, blocking cell communication and tau proteins tangle inside neurons, disrupting nutrient transport (P, Vellapandian, 2024). After surveying existing literature, we seek to better understand the risk factors that influence these biomarkers and the mechanistic pathways that drive AD progression. With age serving as theprimary risk factor, with those over 65 most affected, looking at earlier adulthood allows us to assess the potential role that chronic stress plays in AD pathology throughhypothalamic-pituitary-adrenal (HPA) axis dysregulation and neuroinflammation.