Therapeutic and mechanistic effects of curcumin in huntington’s disease

Curcumin is a spice derived nutraceutical which gained tremendous attention be-cause of its profound medicinal values. It alters a number of molecular pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF‐κB), signal transducer and activator of transcription 3 (STAT3), nuclear factor erythroid 2-related factor 2 (Nrf2) and cyclooxygenases-2 (COX‐2), which make it potential therapeutic choice in treating multiple disorders. It also pos-sesses the potential to prevent protein aggregation and thus protect against degeneration of neurons in neurodegenerative disorders including Huntington’s disease (HD). HD is an autosomal dominant disorder linked with altered gene expression which leads to an increase in the size of cytosine, ade-nine and guanine (CAG) trinucleotide repeats, aids in protein aggregation throughout the brain and thus damages neurons. Upstream regulation of oxidative stress and inflammatory cascade are two important factors that drive HD progression. Available therapies just suppress the severity of symp-toms with a number of side effects. Curcumin targets multiple mechanisms in treating or preventing HD including antioxidant and anti-inflammatory potential, metal ion chelation, transcriptional alterations and upregulating activity of molecular chaperons, heat shock proteins (HSPs). Having a favorable safety profile, curcumin can be an alternative therapeutic choice in treating neurodegen-erative disorders like HD. This review will focus on mechanistic aspects of curcumin in treating or preventing HD and its potential to arrest disease progression and will open new dimensions for safe and effective therapeutic agents in diminishing HD.