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Treatment with controlled-release lovastatin decreases serum concentrations of human beta-amyloid (A beta) peptide.

Author: BuxbaumJ D, CullenE I, FriedhoffL T, GeoghagenN S

Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.
Clinical TrialA clinical trial is a planned study conducted on humans to evaluate the efficacy and safety of pharmaceuticals, medical devices, and treatment methods. It aims to explore the possibilities of new treatments and improve the health of patients.
Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Randomized Controlled TrialA clinical trial that randomly assigns participants to treatment and control groups to evaluate the effects of an intervention.
Research Support, U.S. Gov't, P.H.S.Research funding provided by the Public Health Service (PHS).

Overview

Beta-amyloid (A beta) buildup in the brain is thought to be central to the development of Alzheimer’s disease. Previous studies have shown that lovastatin, a cholesterol-lowering drug, can reduce A beta production in lab settings. This study investigated the effect of lovastatin on A beta levels in living subjects. Individuals with high cholesterol levels were randomly given either lovastatin or placebo for up to 3 months. A dose-dependent decrease in serum A beta levels was observed, with statistically significant differences between the higher lovastatin doses and placebo.
Paper Details　
Original Abstract of the Article :
The deposition of beta-amyloid (A beta) in neuronal plaques is believed to be crucial for the initiation and progression of Alzheimer's disease (AD). Studies in vitro have shown that inhibiting cholesterol metabolism with lovastatin, or its active metabolite lovastatin acid, lowers A beta production...See full text at original site
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引用元：
https://pubmed.ncbi.nlm.nih.gov/11466161

データ提供：米国国立医学図書館（NLM）

Lowering Beta-Amyloid Levels: A Potential Strategy for Alzheimer's Disease

Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by the accumulation of beta-amyloid (A beta) plaques in the brain. This study investigates the effect of lovastatin, a cholesterol-lowering drug, on serum A beta levels in humans. The researchers conducted a double-blind, randomized, placebo-controlled trial involving individuals with elevated cholesterol. Participants received various doses of controlled-release lovastatin or placebo for up to 3 months. The study found a dose-dependent decrease in serum A beta levels in the lovastatin-treated groups, suggesting that lovastatin may have a beneficial effect on A beta levels. However, further research is needed to determine the long-term implications of this finding on AD progression.

Lovastatin: A Potential Player in Alzheimer's Disease?

This study provides intriguing evidence that lovastatin, a commonly prescribed cholesterol-lowering drug, might have a potential role in managing Alzheimer's disease. The observed dose-dependent decrease in serum A beta levels in the lovastatin-treated groups warrants further investigation into the potential therapeutic effects of lovastatin in AD.

Cholesterol Management and Brain Health

This research highlights the potential link between cholesterol management and brain health. While further studies are needed to confirm the specific mechanisms involved, the findings suggest that controlling cholesterol levels may play a role in reducing A beta accumulation and potentially mitigating the progression of Alzheimer's disease.

Dr. Camel's Conclusion

Alzheimer's disease is a complex and challenging condition with no cure. This study offers a glimmer of hope, suggesting that an existing drug, lovastatin, might have a beneficial effect on beta-amyloid levels. While further research is needed to validate these findings and explore potential clinical applications, this study underscores the potential of targeting cholesterol metabolism as a therapeutic strategy for Alzheimer's disease.

Date :
  1. Date Completed 2001-08-16
  2. Date Revised 2022-03-30
Further Info :

Pubmed ID

11466161

DOI: Digital Object Identifier

S1461145701002310

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Languages

English

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