The result indicated that CSF ApoE might aggravate Aβ deposition in the brain (Bales et al., 1999) by acting as “pathological molecular chaperones” (Wisniewski and Frangione, 1992) to promote insolubility or neurotoxicity of CSF Aβ in the early stage of AD pathology (Hudry et al., 2019) and (or) by disrupting Aβ clearance process by competing for the same clearance pathways of soluble Aβ (Verghese et al., 2013). Here, APOE is linked to Alzheimer disease.