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

SERUM amyloid P component (SAP) is associated with amyloid β (Aβ) 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 Aβ deposits in a transgenic mouse model overexpressing β-protein precursor (βPP). Both SAP and another extracellular matrix binding protein, basic fibroblastic growth factor bind to the heparinase sensitive sites of Aβ 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 Aβ deposition, and that this mouse model does not develop the same BBB abnormalities as those seen in AD.