Hepatocyte‐specific LRP1 silencing exacerbates brain amyloidosis without compensatory LDL receptor family involvement

Hepatic LRP1-mediated clearance of peripheral Aβ plays an important role in mitigating brain amyloidosis. Hepatic downregulation of LRP1 in AD mice correlates with increased brain amyloidosis that is neither the result of compensation in other hepatic LDL receptors nor changes in receptors involved in Aβ clearance. Hepatic LRP1 specifically may hold promise as a therapeutic target, especially in conditions resulting in liver damage and hepatic LRP1 reduction such as obesity and alcoholism, known modifiable risk factors for AD.