In this study, we, for the first time, investigated the abnormal alterations of plasma Aβ42, plasma Aβ42/Aβ40, plasma p-Tau181, plasma GFAP, plasma NfL, Aβ PET, tau PET, hippocampal volume, and AD-signature cortical thickness across the different clinical stages of AD based on a Chinese aging cohort in Guangdong-Hong Kong-Macao Greater-Bay-Area. The gene discussed is GFAP; the disease is Alzheimer disease.