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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

Bergamaschini, Luigi, Rossi, Emanuela, Storini, Claudio, Pizzimenti, Simone, Distaso, Maria, Perego, Carlo, De Luigi, Ada, Vergani, Carlo, Grazia De Simoni, Maria·2004·The Journal of Neuroscience
DOI 10.1523/jneurosci.0550-04.2004
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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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Figures

Figure 1 ENO reduces the antibody load in APP23 mice. Representative photomicrographs of 40 𝛍 mprefrontal cortex slices preparedfromAPP23transgenicmiceareshown.ImmunostainingforA 𝛃 revealedfewsmallamyloiddepositsinmicetreatedwithENO ( A ) but several deposits in mice given saline ( B ). Scale bar, 200 𝛍 m. C -E , In cortex slices of APP23 mice treated with ENO or saline, the A 𝛃 load was quantified by evaluating the number of A 𝛃 deposits (horizontal bar indicates the median; * p < 0.02 vs saline; Student's t test) ( C ), the total area occupied by deposits (mean ± SE; * p < 0.03 vs saline; Student's t test) ( D ), and the total, soluble plus insoluble, A 𝛃 (1-40)concentration (horizontal bar indicates the mean; *** p < 0.001 vs saline; Student's t test) ( E ).
Figure 1 ENO reduces the antibody load in APP23 mice. Representative photomicrographs of 40 𝛍 mprefrontal cortex slices preparedfromAPP23transgenicmiceareshown.ImmunostainingforA 𝛃 revealedfewsmallamyloiddepositsinmicetreatedwithENO ( A ) but several deposits in mice given saline ( B ). Scale bar, 200 𝛍 m. C -E , In cortex slices of APP23 mice treated with ENO or saline, the A 𝛃 load was quantified by evaluating the number of A 𝛃 deposits (horizontal bar indicates the median; * p < 0.02 vs saline; Student's t test) ( C ), the total area occupied by deposits (mean ± SE; * p < 0.03 vs saline; Student's t test) ( D ), and the total, soluble plus insoluble, A 𝛃 (1-40)concentration (horizontal bar indicates the mean; *** p < 0.001 vs saline; Student's t test) ( E ).CC-BY-NC-SA · From the PDF
Figure 2 ENO reduces astrocyte activation in APP23 mice. Shown are representative photomicrographs of 40 𝛍 mprefrontal cortex slices prepared from APP23 transgenic mice, showing GFAP-immunopositive astrocytes. Activated astrocytes with enlarged cell bodies and highly ramified, thick processes surround fibrillar amyloid deposits (stained with Congo Red) in APP23 mice treated with saline ( A , C ). Only a few, scattered GFAP-positive cells can be observed in APP23 mice treated with ENO ( B , D ), indicating that the treatment markedly reduced astrocyte activation. Scale bar, 100 𝛍 m.
Figure 2 ENO reduces astrocyte activation in APP23 mice. Shown are representative photomicrographs of 40 𝛍 mprefrontal cortex slices prepared from APP23 transgenic mice, showing GFAP-immunopositive astrocytes. Activated astrocytes with enlarged cell bodies and highly ramified, thick processes surround fibrillar amyloid deposits (stained with Congo Red) in APP23 mice treated with saline ( A , C ). Only a few, scattered GFAP-positive cells can be observed in APP23 mice treated with ENO ( B , D ), indicating that the treatment markedly reduced astrocyte activation. Scale bar, 100 𝛍 m.CC-BY-NC-SA · From the PDF
Figure 3 ENO dose-dependently attenuates A 𝛃 (1-40) cytotoxicity. The viability of differentiated PC12 cells was measured by densitometric analysis of surviving cells stained with MTT. Cells (15 × 10 3 /cm 2 ) were exposed to A 𝛃 (1-40) (25 𝛍 M) or A 𝛃 plus ENO at different concentrations (1, 5, and 10 mM) for 72 hr. Data are the mean ± SE optical density (O.D.). (** p < 0.01; *** p < 0.001 vs A 𝛃 alone; ANOVA followed by Tukey's test).
Figure 3 ENO dose-dependently attenuates A 𝛃 (1-40) cytotoxicity. The viability of differentiated PC12 cells was measured by densitometric analysis of surviving cells stained with MTT. Cells (15 × 10 3 /cm 2 ) were exposed to A 𝛃 (1-40) (25 𝛍 M) or A 𝛃 plus ENO at different concentrations (1, 5, and 10 mM) for 72 hr. Data are the mean ± SE optical density (O.D.). (** p < 0.01; *** p < 0.001 vs A 𝛃 alone; ANOVA followed by Tukey's test).CC-BY-NC-SA · From the PDF
Image 4
CC-BY-NC-SA · From the PDF
Image 5
CC-BY-NC-SA · From the PDF
Figure 4 ENO inhibits A 𝛃 (1-40)-dependent activation of the complement and contact systems. Shown is representative SDS-PAGE and Western blotting analysis of the cleavage of C4 ( A ) and HK ( B ) as indicators of complement and contact system activation, respectively. At the bottom of each lane, the percentages of cleaved C4 (C4c vs C4 plus C4c) and HK (bands II and III vs I plus II and III) were determined by densitometric analysis of the immunostained membrane. ENO but not DS or HS caused dose-dependent inhibition of the cleavage of C4 and HK induced by A 𝛃 (25 𝛍 M). Columns show the mean ± SE (%) of C4 ( C ) and HK( D ) cleavage in three separate experiments run in triplicate (** p > 0.01; *** p > 0.001 vs A 𝛃 alone; Kruskal-Wallis followed by Dunn's test).
Figure 4 ENO inhibits A 𝛃 (1-40)-dependent activation of the complement and contact systems. Shown is representative SDS-PAGE and Western blotting analysis of the cleavage of C4 ( A ) and HK ( B ) as indicators of complement and contact system activation, respectively. At the bottom of each lane, the percentages of cleaved C4 (C4c vs C4 plus C4c) and HK (bands II and III vs I plus II and III) were determined by densitometric analysis of the immunostained membrane. ENO but not DS or HS caused dose-dependent inhibition of the cleavage of C4 and HK induced by A 𝛃 (25 𝛍 M). Columns show the mean ± SE (%) of C4 ( C ) and HK( D ) cleavage in three separate experiments run in triplicate (** p > 0.01; *** p > 0.001 vs A 𝛃 alone; Kruskal-Wallis followed by Dunn's test).CC-BY-NC-SA · From the PDF
Image 7
CC-BY-NC-SA · From the PDF

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Citations

Cites

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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
DOI
10.1523/jneurosci.0550-04.2004
Cited by
146
References
8
Language
en
Licence
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)

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