LAUSR

Alzheimer’s disease (AD) is the leading cause of dementia in the elderly, representing 60–70% of cases, with a prevalence of 10% in people aged 65 and older [1]. AD has a complex and heterogeneous nature and is characterized by a slow but inexorable neuronal death that involves a vast area of the central nervous system (CNS), including hippocampus, amygdala and several cortical areas, including para-hippocampal, entorhinal and frontal. Copper (Cu) not bound to ceruloplasmin (non-ceruloplasmin Cu, also known as ‘free’ Cu), higher than 1.6 μM in serum/plasma, has been recently shown to be a risk factor in subjects with mild cognitive impairment (MCI), accelerating progression to frank AD [2]. This point of view article focuses on the role of Cu in brain physiology and pathology trying to understand how to possibly intervene in order to reduce the accelerating role of copper in AD. The systemic role of Cu