Title:Therapeutic and Mechanistic Effects of Curcumin in Huntington’s Disease
Volume: 19
Issue: 7
Author(s): Fabiana Labanca, Hammad Ullah, Haroon Khan*, Luigi Milella, Jianbo Xiao, Zora Dajic-Stevanovic and Philippe Jeandet
Affiliation:
- Department of Pharmacy, Abdul Wali Khan University Mardan, 23200,Pakistan
Keywords:
Curcumin, huntington's disease, therapeutic potential, degenerative diseases, oxidative stress, neuroinflammation,
underlying mechanisms.
Abstract: Curcumin is a spice derived nutraceutical which gained tremendous attention because
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 possesses
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, adenine
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 symptoms
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 neurodegenerative
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.