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Blood-borne ?-amyloids (A?s) could affect brain function by (1) crossing the BBB to directly interact with brain tissues or (2) altering BBB function by interacting with the brain capillaries that make up the BBB. Several radioactively labeled A?e have been examined for such interactions. Blood-borne A?1-28is hindered from accumulating in brain by a slow rate of passage across the BBB and by robust enzymatic degradation. A?1-40, but not A?40-1or A?1-42, is sequestered by brain capillaries, raising the possibility that it could affect BBB function. Small amounts of circulating A?1-40are recovered intact from CSF and brain. A?1-40is degraded by aluminum-sensitive, calcium-dependent intracellular enzymes. Apo-J, which can bind A?, has been shown with an in situmethod to be transported by a saturable system across the BBB. However, our recent work has shown that this system is not operable in vivo, probably because the transporter is saturated at physiological blood levels. In conclusion, A?s have been shown to interact with and to cross the BBB.