In conclusion, the present study highlighted the neuroprotective potential of cilostazol against 3-NP-induced HD model via modulating the crosstalk between TLR-4, Akt/GSK-3β/CREB and JAK-2/STAT3/SOCS-3 signalling pathways to provide a promising therapeutic tool slowing the progression of HD. Here, GSK3B is linked to Huntington disease.