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Lovastatin enhances Abeta production and senile plaque deposition in female Tg2576 mice


Year of Publication:
Contact PI Name:
Inhee Mook-Jung
Contact PI Affiliation:
Brain Disease Research Center, Ajou University School of Medicine, Suwon, South Korea
In-Ho Park, Eun Mi Hwang, Hyun Seok Hong, Jung Hyun Boo, Sang Soo Oh, Jeewoo Lee, Min Whan Jung, Oh Young Bang, Seung U. Kim
Primary Reference (PubMED ID):
Funding Source:
Korean Ministry of Science and Technology (MoST)
Study Goal and Principal Findings:

Data from a number of epidemiological studies suggest that cholesterol levels might be related to risk for AD. In addition, data from a number of  studies employing animal models of AD suggest that cholesterol modulates APP processing and consequently alters Aβ production and senile plaque deposition. Based on these lines of evidence,  investigators, in this study, used the Tg2576 AD mouse model to explore the interaction between cholesterol and AD-like neuropathology. The authors separately examined the effects of lovastatin on cholesterol level on APP processing beta-amyloid production and senile plaque deposition, in male and female mice.Lovastatin lowered  plasma cholesterol levels in both genders.  The major findings of this study are:1) lovastatin lowered  plasma cholesterol levels in both genders; 2) lovastatin enhanced the amounts of β-amyloid and other β-secretase derived peptides in females, but not in males;3) lovastatin increased the number of plaques in the hippocampus and cortex of females, but not in males; 4) lovastatin did not change the amounts of full-length or α-secretase processed APP or, PS1 in either sex. Thus, lovastatin lowers cholesterol level in both genders, but enhances β-amyloid production and senile plaque deposition only in brains of female Tg2576 mice. These results suggest that low cholesterol might be a risk factor for AD in females.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
Therapeutic Target:
HMG-CoA Reductase

Animal Model

Model Information:
Model Type:
Strain/Genetic Background:
Not Reported

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest


Outcome Measured
Outcome Parameters
beta Amyloid Deposits
Brain-beta Amyloid Peptide-Total
Amyloid Precursor Protein (APP)
Amyloid Precursor Protein (APP) Metabolites
Presenilin 1 (PS1)
Target Engagement (Reduction Total Cholesterol-Plasma)
Body Weight
Food Intake