IBRO Neuroscience Reports (Dec 2024)
Effects silymarin and rosuvastatin on amyloid-carriers level in dyslipidemic Alzheimer’s patients: A double-blind placebo-controlled randomized clinical trial
Abstract
Purpose: The production/excretion rate of Amyloid-β (Aβ) is the basis of the plaque burden in alzheimer's disease (AD), which depends on both central and peripheral clearance. In this study, the effect of silymarin and rosuvastatin on serum markers and clinical outcomes in dyslipidemic AD patients was investigated. Methods: Participants (n=36) were randomized to silymarin (140 mg), placebo, and rosuvastatin 10 mg orally three times a day for 6 months. Serum collection and clinical outcome tests were performed at baseline and after completion of treatment. Lipid profile markers, oxidative stress markers, Aβ1–42/Aβ1–40 ratio, and Soluble Low-density lipoprotein receptor-Related Protein-1 (sLRP1)/Soluble Receptor for Advanced Glycation End Products (sRAGE) ratio were measured. Results: There was a statistically significant increase in Δ-high density lipoprotein (ΔHDL) between silymarin and placebo (P<0.000) and also between rosuvastatin and placebo (p=0.044). The level of Δ-triglycerides (ΔTG) in the silymarin group has a significant decrease compared to both the placebo and the rosuvastatin group (p<0.000 and p=0.036, respectively). The Δ-superoxide dismutase (ΔSOD) level in the silymarin group compared to placebo and rosuvastatin had a significant increase (p<0.000 and p=0.008, respectively). The ΔAβ1–42/Aβ1–40 in the silymarin group compared to both the placebo and rosuvastatin groups had a significant increase (p<0.05). There was an inverse relationship between ΔTG and ΔAβ1–42/Aβ1–40 (p=-0.493 and p=0.004). ΔAβ1–42/Aβ1–40 has a direct statistical relationship with ΔSOD marker (p=0.388 and p=0.031). Also, there was a direct correlation between the level of ΔAβ1–42/Aβ1–40 and ΔsLRP1/sRAGE (p=0.491 and p=0.005). Conclusion: Our study showed the relationship between plasma lipids, especially ΔTG and ΔHDL, with ΔAβ1–42/Aβ1–40 in dyslipidemic AD patients, and modulation of these lipid factors can be used to monitor the response to treatments.
