Host oxidative stress pathways and amyloid-beta accumulation

Host oxidative stress pathways and amyloid-beta accumulation refers to the reciprocal relationship between the generation of reactive oxygen species (ROS) and the aggregation of amyloid-beta (Aβ) peptides, primarily in the context of Alzheimer's disease. Oxidative stress occurs when the production of free radicals exceeds the capacity of cellular antioxidant defenses, leading to damage of essential macromolecules (Butterfield et al., 2013). Aβ accumulation, a hallmark of neurodegeneration, promotes oxidative stress by disrupting mitochondrial membranes and activating inflammatory pathways in microglia (Butterfield & Boyd-Kimball, 2018). Conversely, oxidative stress can stimulate the amyloidogenic processing of amyloid precursor protein (APP) by increasing the expression and activity of beta-secretase (BACE1) (Chen & Zhong, 2014). Therapeutic interventions targeting this axis include monoclonal antibodies designed to clear Aβ plaques and various antioxidant compounds aimed at restoring redox balance (Jack et al., 2018). However, because this term encompasses a broad set of biological processes and multiple molecular species, it is classified as a pathological mechanism rather than a single therapeutic target.

Other names

Oxidative stress-induced amyloidogenesisROS-Aβ axisAmyloid-beta and oxidative stress interplayRedox imbalance in Alzheimer's disease

Reduction of reactive oxygen species (ROS), inhibition of Aβ aggregation, clearance of Aβ plaques, and activation of antioxidant response elements (ARE).