Figure 4.

Possible brain Aβ clearance mechanisms. Aβ peptides may be removed by enzymatic degradation within brain parenchyma [38, 173] or they can be transported through the blood-brain-barrier into the blood or CSF by receptor for advanced glycation endproducts (RAGE), ApoE, β-2-macroglobulin, and the low-density lipoprotein receptor (LRP) [3, 174–176]. The steady-state level of brain Aβ depends upon a balance between production and catabolism. Increased production (like in familial AD) and/or decreased clearance (for most sporadic AD) will result in elevated brain Aβ levels and potentially trigger or accelerate the pathogenesis of AD. RAGE: receptor for advanced glycation end products; LRP: low-density lipoprotein receptor-related protein.