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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Serum amyloid P is not present in amyloid beta deposits of a transgenic animal model.

Serum amyloid P component (SAP) is associated with amyloid beta ( A beta) deposition in Alzheimer disease (AD). Since SAP is exclusively synthesized by peripheral organs, its presence in the brain of AD suggests impairment of the blood-brain barrier (BBB). We studied the association of SAP with A beta deposits in a transgenic mouse model overexpressing beta-protein precursor (betaPP). Both SAP and another extracellular matrix binding protein, basic fibroblastic growth factor bind to the heparinase sensitive sites of A beta deposits in this model. However, no endogenous SAP immunoreactivity was found in the transgenic mouse brain. These results suggest that SAP is not required for A beta deposition, and that this mouse model does not develop the same BBB abnormalities as those seen in AD.[1]

References

  1. Serum amyloid P is not present in amyloid beta deposits of a transgenic animal model. Shi, J., Perry, G., Aliev, G., Smith, M.A., Ashe, K.H., Friedland, R.P. Neuroreport (1999) [Pubmed]
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