Lastly, further research is warranted to unravel AD-specific effects of neurotoxic proteins, their potential interactions with ApoE ε4/Aβ, the possible wide-ranging physiological and pathological roles of LRP1 and TIMP3 in AD pathogenesis as well as the development of potential treatment approaches to prevent or repair ApoE ε4-related BBB impairments. This evidence concerns the gene LRP1 and Alzheimer disease.