Amyloid plaques, neurofibrillary tangles and neuro-inflammation are the hallmarks of Alzheimer’s disease. Several mediators in the inflammation cascade contribute to neurodegeneration as well as the production and accumulation of the β-amyloid peptide, interleukin 1β (IL-1β), reactive oxygen species, inducible nitric oxide synthase (iNOS) and lipid peroxidation products (Akiyama et al., 2000). Considerable attention has been directed towards identifying compounds with neuroprotective properties.
Tetrahydrocurcumin (THC) caused inhibition of iNOS protein mRNA and IL-1β in lipopolysaccharide (LPS)-induced inflammation in the brain tissue of THC-treated mice and the EC50 values were highly significant. Soluble amyloid-β seems to closely correlate with synaptic loss and neurodegeneration in Alzheimer’s disease and THC reduced it by 75% (Frautschy et al., 2001).
Recent studies reveal the benefits of THC in protecting neurons against amyloid-β-induced toxicity by reducing the amyloid-β-induced: