β-amyloid and oxidative stress: perspectives in drug development

Alzheimer's Disease (AD) is a slow-developing neurodegenerative disorder in which a main pathogenic role has been assigned to β-amyloid protein (Aβ) that accumulates in extracellular plaques. The mechanism of action of Aβ has been deeply analyzed and several membrane structure have been identified as potential mediators of its effect. The ability of Aβ to modify neuronal activity, receptor expression, signaling pathways, mitochondrial function, and involvement of glial cells have been analyzed. In addition, a large body of the literature deals with the involvement of oxidative stress in Aβ effects. We here focus more specifically on the reciprocal regulation of Aβ, that causes oxidative stress, and oxidative stress, that favors Aβ aggregation and toxicity and negatively affects the peptide clearance. Analysis of this strict interaction may offer novel opportunities for therapeutic intervention. Common as well as new molecules endowed with antioxidant properties deserve attention in this regard.