Abstract
Amyloid β (Aβ) accumulates in the neuropil and within the walls of cerebral vessels in association with normal aging, dementia or stroke. Aβ is released from its precursor protein as soluble monomeric species yet, under pathological conditions, it self-aggregates to form soluble oligomers or insoluble fibrils that may be toxic to neurons and vascular cells. Aβ levels could be lowered by inhibiting its generation or by promoting its clearance by transport or degradation. Here we will summarize recent findings on brain proteases capable of degrading Aβ, with a special focus on those enzymes for which there is genetic, transgenic or biochemical evidence supporting a role in the proteolysis of Aβ in vivo.
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Morelli, L., Bulloj, A., Leal, M.C., Castaño, E.M. (2005). Amyloid β Degradation: A Challenging Task for Brain Peptidases. In: Harris, J.R., Fahrenholz, F. (eds) Alzheimer’s Disease. Subcellular Biochemistry, vol 38. Springer, Boston, MA . https://doi.org/10.1007/0-387-23226-5_6
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