Abstract
It is estimated that Alzheimer’s disease (AD) is striking 1 in 20 over age 65, which yielded to 23–35 million people worldwide in 2015. The number of AD victims is expected to almost double every 20 years, thus placing the national healthcare systems under dramatically increasing pressure. This clearly underlines the need to find early biomarkers and efficient medical treatments for AD, both implying a better understanding of the mechanism from the origin of the disease to the death of the neurons. Oxidative damages on neuronal lipids and proteins, in particular, are an important feature of AD and a link with oxidative stress [1]. The latter can have different origins, but the overproduction of reactive oxygen species (ROS) is considered as a major contribution. Loosely bound metal ions (copper and iron), present in the brain and at high concentration in senile plaques of AD patients, may bind to the amyloid beta peptide (Aβ) thus catalyzing very efficiently the production of ROS (in particular, the oligomeric forms of Aβ, known as being the most toxic). This represents one of the source for ROS production in brain, a second one being mitochondria dysfunction.