For example, elevated levels of FPP and GGPP were observed in the brains of AD patients, and suppression of FTase or GGTase-I could mitigate Aβ-associated neuropathology in an AD mouse model.293 In another study, upregulated expression of FT and H-Ras farnesylation was observed in AD brains and the upregulation of FT and H-Ras farnesylation was associated with mild cognitive impairment, indicating that abnormal regulation of protein prenylation is involved in the AD pathogenic cascade. This evidence concerns the gene HRAS and Alzheimer disease.