Berberine can be a Potential Therapeutic Agent in Treatment of Huntington's Disease: A Proposed Mechanistic Insight
Abstract
Huntington's disease (HD) is a genetic neurodegenerative disorder caused by CAG repeat expansion in the HTT gene, producing mutant huntingtin (mHTT) protein. This leads to neuronal damage through protein aggregation, transcriptional dysregulation, excitotoxicity, and mitochondrial dysfunction. mHTT impairs protein clearance and alters gene expression, energy metabolism, and synaptic function. Therapeutic strategies include enhancing mHTT degradation, gene silencing via antisense oligonucleotides and RNAi, promoting neuroprotection through BDNF signaling, and modulating neurotransmitters like glutamate and dopamine. Berberine, a natural isoquinoline alkaloid, has emerged as a promising therapeutic option for HD due to its multifaceted neuroprotective properties. Research indicates that berberine can mitigate the progression of neurodegenerative diseases, including HD, by targeting various molecular pathways. It exhibits antioxidant, anti-inflammatory, and autophagy-enhancing effects, which are crucial in reducing neuronal damage and apoptosis associated with HD. These properties make berberine a potential candidate for therapeutic intervention in HD, as demonstrated in both cellular and animal models. Berberine activates the PI3K/Akt pathway, which is vital for cell survival and neuroprotection. It reduces oxidative stress and neuroinflammation, both of which are implicated in HD pathology. Berberine enhances autophagic processes, promoting the degradation of mutant…
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