ABSTRACT
The deleterious effect of oxidative stress in some neurodegenerative disorders (NDDs) such as Alzheimer's disease (AD) or Parkinson's diseases (PD) is well established. For instance, lipid peroxidation, protein oxidation, and nucleic acid oxidation damage markers were found to be elevated while antioxidant levels decreased in vulnerable region of the brain from patients with NDDs. However, curcumin brain bioavailability is low due to its low stability in solution and its poor permeability across the blood–brain barrier (BBB). In comparison with peripheral capillaries, the brain capillaries do not have fenestrations and microvessel endothelial cells (MECs) are recovered by pericytes and which confer a more tightly structure. The BBB is characterized by the presence of tight junctions (TJs) between MECs which induce a high transendothelial electrical restriction. TJs are the most important element in the junctional complex which is formed by transmembranar proteins such as claudins, a protein associated to the regulation of the microenvironment and in the control of cell proliferation.
