Glycosides of Cistanche(GC)is a preparation used extensively for its neuroprotective effect against neurological diseases,but its mechanisms of action remains incompletely understood.Here,we established a bilateral common carotid artery occlusion model of vascular dementia in rats and injected the model rats with a suspension of GC(10 mg/kg/day,intraperitoneally)for 14 consecutive days.Immunohistochemistry showed that GC significantly reduced p-tau and amyloid beta(Aβ)immunoreactivity in the hippocampus of the model rats.Proteomic analysis demonstrated upregulation of mitochondrial precursor protein and downregulation of keratin type II cytoskeletal6A after GC treatment compared with model rats that had received saline.Western blot assay confirmed these findings.Our results suggest that the neuroprotective effect of GC in vascular dementia occurs via the promotion of neuronal cytoskeleton regeneration. Glycosides of Cistanche (GC) is a preparation used extensively for its neuroprotective effect against neurological diseases, but its mechanisms of action remains incompletely. Here, we established a bilateral common carotid artery occlusion model of vascular dementia in rats and injected the model rats with a suspension of GC (10 mg / kg / day, intraperitoneally) for 14 consecutive days. Immunohistochemistry showed that GC significantly reduced p-tau and amyloid beta (Aβ) immunoreactivity in the hippocampus of the model rats. Protein analysis demonstrated upregulation of mitochondrial precursor protein and downregulation of keratin type II cytoskeletal 6A after GC treatment compared with model rats that had received saline. Western blot assay confirmed these findings. Our results suggest that the neuroprotective effect of GC in vascular dementia occurs via the promotion of neuronal cytoskeleton regeneration.