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Peripheral treatment with enoxaparin, a low molecular weight heparin, reduces plaques and beta-amyloid accumulation in a mouse model of Alzheimer's disease


Year of Publication:
Contact PI Name:
Luigi Bergamaschini
Contact PI Affiliation:
Department of Internal Medicine, Ospedale Maggiore, Instituto di Ricovero e Cura a Carattere Scientifico, University of Milan, Milan, Italy
Emanuela Rossi, Claudio Storini, Simone Pizzimenti, Maria Distaso, Carlo Perego, Ada De Luigi, Carlo Vergani, Maria Grazia De Simoni
Primary Reference (PubMED ID):
Funding Source:
Ministero della Sanita Italy
Fondazione Monzino Italy
Study Goal and Principal Findings:

This study investigated the effect of long-term, peripheral treatment with enoxaparin, a low molecular weight heparin, in transgenic mice overexpressing human amyloid precursor protein751. Enoxaparin (6 IU per mouse intraperitoneally, three times a week for 6 months) significantly lowered the number and the area occupied by cortical -amyloid deposits and the total β-amyloid (1– 40) cortical concentration. Immunocytochemical analysis of glial fibrillary acid protein-positive cells showed that enoxaparin markedly reduced the number of activated astrocytes surrounding -amyloid deposits.In vitro, the drug dose-dependently attenuated the toxic effect of β-amyloid on neuronal cells. Enoxaparin dose-dependently reduced the ability of β-amyloid to activate complement and contact systems, two powerful effectors of inflammatory response in AD brain. By reducing the β-amyloid load and cytotoxicity and proinflammatory activity, enoxaparin offers promise as a tool for slowing the progression of Alzheimer’s disease.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Small Molecule
Therapeutic Agent:
Enoxaparin (ENO)
Therapeutic Target:
Antithrombin III

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 Load
Brain-beta Amyloid Peptide 40
Complement Activation
Gene Expression Profile-Inflammatory Genes
Glial Fibrillary Acidic Protein (GFAP)
Brain-beta Amyloid Deposits
Activated Astrocytes
Cell Biology
Electron Microscopy
Aggregated beta Amyloid Peptide