Neuroinflammation, marked by activation of the brain's resident immune cells (microglia), is now recognized as an early feature of HD that may actively worsen disease progression, not just a byproduct of neuronal death. Mutant huntingtin protein is expressed in microglia themselves and alters how these cells respond to inflammatory signals. HD-positive individuals also show elevated systemic inflammatory markers, including interleukin-6, that can be detected years before clinical symptom onset — raising the possibility of anti-inflammatory approaches as a complementary strategy alongside huntingtin-lowering therapies, and of inflammatory biomarkers as an early detection tool.