Chapter 23 - Curcumin against amyloid pathology in mental health and brain composition

Abstract

Recent evidence suggests that amyloid pathology occurs 10–20 years before the clinical onset of Alzheimer’s disease (AD). Accordingly, modulating abnormal amyloid-β (Aβ) aggregation is now considered as a potential therapeutic target in AD. Curcumin, a low molecular weight polyphenol derived from the well-known spice turmeric, has various pharmacological properties, including antitumor, antioxidative, antiinflammatory, and antiamyloid effects. Curcumin binds both Aβ fibrils and oligomers and inhibits Aβ aggregation as well as Aβ-related oxidative stress and inflammation. The keto–enol tautomerism of curcumin is involved in its binding to Aβ aggregates. The enol form, but not the keto form, of curcumin can bind to Aβ aggregates. When curcumin was administered to transgenic mouse models of AD, it effectively suppressed amyloid pathology in the mouse brain. However, the results of early clinical trials of curcumin for AD have been negative, probably due to its low bioavailability. Several approaches have been proposed to improve the bioavailability of curcumin.