[14] Moreover, apoA‐I deficiency tends to accelerate cognitive decline in AD progress, while increased apoA‐I level will improve cognitive function and alleviate neuroinflammation through multiple mechanisms.[15] As a result, apoA‐I‐enriched nanocarriers possess tremendous potential for AD treatment.[16] The structure of the amphipathic α‐helical repeats promotes apoA‐I to insert into the lipid layer and form a protein–lipid nanocomposite (PLN).[17] The biomimetic PLN can perform as a drug carrier for multidrug shielding, and maintain the high binding affinity to Aβ. Here, APOA1 is linked to Alzheimer disease.