Second, we found that NAFLD hindered the hepatic uptake of Aβ via the PPARα/LRP-1 pathway, but studies in hepatocyte-specific LRP-1 or PPARα overexpression animal models challenged with a long-term HFD are required to clarify its role in NAFLD-induced Aβ pathology and cognitive impairment. The gene discussed is LRP1; the disease is metabolic dysfunction-associated steatotic liver disease.