Curcumin is a phenolic compound that can be extracted from the curcuma rhizome. It has low toxicity, along with anti-inflammatory, antibiosis, and anti-oxidative properties, with few side effects. Because curcumin is liposoluble, it can pass through the blood-brain barrier. Moreover, as a peroxisome proliferator-activated receptor-γ agonist, curcumin can significantly inhibit amyloid beta production and aggregation, and reduce inflammation and oxidative damage in Alzheimer’s disease. Additionally, curcumin has strong neuroprotective effects. However, the mechanism of action remains poorly understood.
In this issue of NRR, four papers have discussed neuroprotection conferred by curcumin with respect to anti-inflammation, anti-oxidation, calcium overload inhibition, and promotion of the expression of nestin and glial fibrillary acidic proteins. The activity of beta-site APP cleaving enzyme 1 and expression level of peroxisome proliferator-activated receptor-γ were determined to investigate the inhibitory effects of curcumin on beta-amyloid protein 40/42.
l Protective effect of curcumin on tumor necrosis factor-alpha-induced neuronal damage in the rat hippocampus: a relationship to the inhibition of neuronal Ca²⁺ influx
Neural Regen Res. 2010;5(2): 113-117.       
l Curcumin reduces inflammatory reactions following transient cerebral ischemia/reperfusion injury
Neural Regen Res. 2011;6(3): 219-223.
l Curcumin alters expression of glial fibrillary acidic protein and nestin following chronic cerebral ischemia
Neural Regen Res. 2011;6(9): 651-655.
l Curcumin inhibits beta-amyloid protein 40/42 expression in the brain in a concentration- and time-dependent manner
Neural Regen Res. 2010;5(16): 1205-1210.