Huntington’s disease is a progressive, autosomal dominant neurodegenerative disorder caused by expanded CAG trinucleotide repeats in the HTT gene, resulting in a mutant huntingtin protein. The mutant protein undergoes misfolding and intraneuronal aggregation, leading to transcriptional dysregulation of neuronal survival genes, mitochondrial dysfunction, and defective autophagic clearance of protein aggregates. These toxic aggregates also activate microglia and astrocytes, triggering chronic neuroinflammation. Despite advances in understanding pathology, there is currently no cure, and treatment is symptomatic. Emerging therapeutic strategies, including gene-silencing approaches such as antisense oligonucleotides, RNA interference, and gene editing, are pursued to lower HTT expression. Autophagy enhancers and novel peptide-brush polymer scaffolds are investigated to promote mutant HTT clearance. Immunomodulatory agents aim to mitigate glial activation and inflammation. These diverse strategies underscore the translational relevance of mechanistic perceptions in cellular pathogenesis. These pave the way to targeted neuroprotective and disease-modifying therapeutic development. This chapter highlights the molecular underpinnings of Huntington’s disease and explores emerging therapeutic avenues, emphasizing the potential for translating mechanistic insights into targeted, disease-modifying interventions.