There is emerging evidence that associates neurological degeneration in Huntington’s disease with cellular senescence characterized by permanent arrest in cell cycling and secretion of pro-inflammatory substances. Repetition of CAG trinucleotides of the HTT gene is associated with Huntington’s disease, a severe autosomal-dominant disorder that affects mitochondrial function, changes redox state, and decreases genomic stability due to mutated huntingtin protein. There are growing studies that show that mutant huntingtin (mHTT) accelerates cellular senescence in neuronal and glial cells via the activation of the DNA damage response and triggering of essential senescence pathways including the p53/p21CIP1 and p16INK4a. Also, senescent microglia and astrocytes show an analysis of HD patient and preclinical data that repeatedly identified senescence-related markers such as SA-β-gal, γH2AX, and increased SASP factors. These results show that senescence serves as a pathogenic amplifier in HD, rather than just a side effect of the disease. There are data to support that anti-senescent therapies, including senomorphics through which NF-κB or mTOR can be modulated or senolytics using inhibitors of the BCL-2 family, can help mitigate neurodegenerative action in HD rodent models. Nevertheless, important questions remain unanswered about long-term safety, the best moment for intervention, and selectivity for certain cell types. An enticing possibility for HD modification is through targeting cellular senescence, and increased investigation is necessary to explore better the possibility of it being translated, including in vivo models, biomarker development, and clinical trials.