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Peripheral Treatment with Enoxaparin, a Low Molecular Weight Heparin, Reduces Plaques and β-Amyloid Accumulation in a Mouse Model of Alzheimer's Disease
Abstract
We investigated the effect of long-term, peripheral treatment with enoxaparin, a low molecular weight heparin, in transgenic mice overexpressing human amyloid precursor protein 751 . Enoxaparin (6 IU per mouse intraperitoneally, three times a week for 6 months) significantly lowered the number and the area occupied by cortical β-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 β-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.
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“Bergamaschini et al. demonstrated that the effect of long-term, peripheral treatment with a low-molecular-weight heparin significantly decreased Aβ concentration and deposition in the brain of APP transgenic mice (Bergamaschini et al., 2004).”
From Heparan Sulphate Proteoglycan and the Low-Density Lipoprotein Receptor-Related Protein 1 Constitute Major Pathways for Neuronal Amyloid-β Uptake (2011) · cites this paper as Bergamaschini et al., 2004
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Metadata
- Authors
- Bergamaschini, L., Rossi, E., Storini, C., Pizzimenti, S., Distaso, M., Perego, C., De Luigi, A., Vergani, C., & Grazia De Simoni, M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-04-28
- Volume
- 24
- Issue
- 17
- Pages
- 4181-4186
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 146
- References
- 8
- Language
- en
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