Huntington's disease research is exciting and constantly evolving Gene therapy and gene editing represent a promising avenue that aims to modify the faulty gene that causes HD. Gene therapy involves introducing healthy copies of the huntingtin gene or tools to silence the mutant gene. Gene editing techniques like CRISPR-Cas9 are being explored to directly edit the mutated gene. These approaches are still in early stages of clinical trials, but they hold immense potential for future treatment. 281 RNA silencing focuses on using small molecules called interfering RNA (RNAi) to silence the mutant huntingtin gene. RNAi essentially targets the mutant messenger RNA (mRNA) and prevents it from being translated into the harmful protein. Similar to gene therapy, RNA silencing is undergoing clinical trials to assess its safety and effectiveness. Antisense oligonucleotides (ASOs) are another strategy to target mutant huntingtin mRNA. These are short, single-stranded pieces of DNA designed to bind to the mutant mRNA and prevent its translation into protein. ASOs have shown promise in early studies, and researchers are exploring their potential for HD treatment. Researchers are investigating various cellular processes involved in HD progression. This includes studying the role of protein aggregation, oxidative stress, and inflammation. By targeting the specific molecular pathways with medications, they hope to slow down neurodegeneration. Several drugs targeting these pathways are undergoing clinical trials.