Modulating glymphatic activity may thus enhance the delivery and potency of antisense oligonucleotides in HD treatment, making it a promising avenue for therapeutic exploration.58 Concerning the mechanisms by which mutant huntingtin is cleared from the brain, research has demonstrated that huntingtin enters the CSF through both passive release and active secretion, followed by glymphatic clearance in mice.59 Future studies are likely to elucidate the potential of glymphatic clearance as an early biomarker and a viable therapeutic target for HD. Here, HTT is linked to Huntington disease.