Amyloid beta and hepatic lrp1
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Amyloid-beta (Aβ) metabolism and clearance are intricately linked to hepatic functions, particularly involving the hepatic lipoprotein receptor-related protein 1 (LRP1). Studies suggest that liver steatosis, induced by factors like heavy alcohol consumption or obesity, can modulate hepatic LRP1 expression. Additionally, liver-type fatty acid-binding protein 1 (FABP1) levels are elevated in Alzheimer's disease (AD) patients, showing associations with Aβ and tau levels in plasma and cerebrospinal fluid, indicating a potential role in AD pathogenesis. Furthermore, the liver plays a crucial role in Aβ metabolism, with receptors like LRP1, P-glycoprotein, and RAGE involved in hepatic uptake and biliary excretion of Aβ, suggesting that enhancing Aβ clearance via LRP1 and P-gp induction could be a novel therapeutic approach for AD prevention and treatment.
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| Papers (5) | Insight |
|---|---|
77 Citations | Liver dysfunction, particularly through LRP-1 receptor involvement, may impact amyloid beta clearance, contributing to Alzheimer's progression outside the brain by affecting peripheral clearance pathways. |
| LRP1 plays a major role in hepatic uptake of amyloid-β (Aβ) in rat hepatocytes, contributing to Aβ systemic clearance and suggesting a potential therapeutic target for Alzheimer's disease. | |
| Chronic alcohol intake downregulates hepatic LRP1 and upregulates APP, potentially shifting the liver from Aβ remover to producer, linking liver steatosis to Alzheimer's disease pathology. | |
| The paper discusses hepatic roles in amyloid metabolism but does not specifically address amyloid beta and hepatic LRP1 interaction. "Not addressed in the paper." | |
| Not addressed in the paper. |
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