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From the Department of Physiology and Cellular Biophysics, Columbia University, College of Physicians and Surgeons, New York, New York
In Alzheimer’s disease (AD), fibrillar ß-amyloid protein (fAß) accumulates in the walls of cerebral vessels associated with vascular smooth muscle cells (SMCs), endothelium, and pericytes, and with microglia and astrocytes in plaques in the brain parenchyma. Scavenger receptor class A (SR-A) and class B, type I (SR-BI) mediate binding and ingestion of fAß by cultured human fetal microglia, microglia from newborn mice, and by cultured SMCs. Our findings that SR-BI participates in the adhesion of cultured microglia from newborn SR-A knock-out mice to fAß-coated surfaces, and that microglia secrete reactive oxygen species when they adhere to these surfaces prompted us to explore expression of SR-BI in vivo. We report here that astrocytes and SMCs in normal adult mouse and human brains and in AD brains express SR-BI. In contrast, microglia in normal adult mouse and human brains and in AD brains do not express SR-BI. These findings indicate that SR-BI may mediate interactions between astrocytes or SMCs and fAß, but not of microglia and fAß, in AD, and that expression of SR-BI by rodent microglia is developmentally regulated. They suggest that SR-BI expression also is developmentally regulated in human microglia.
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