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Amyloid β Degradation: A Challenging Task for Brain Peptidases

  • Laura Morelli
  • Ayelén Bulloj
  • María Celeste Leal
  • Eduardo M. Castaño
Chapter
Part of the Subcellular Biochemistry book series (SCBI, volume 38)

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.

Key words

Amyloid β dementia stroke amyloidoses Alzheimer’s disease brain proteases insulin degrading enzyme 

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Copyright information

© Springer Science+Business Media, Inc. 2005

Authors and Affiliations

  • Laura Morelli
    • 1
  • Ayelén Bulloj
    • 1
  • María Celeste Leal
    • 1
  • Eduardo M. Castaño
    • 1
  1. 1.Instituto de Química y Fisicoquímica Biológicas (IQUIFIB), CONICET. Cátedra de Química Biológica Patológica, Departamento de Química Biológica, Facultad de Farmacia y BioquímicaUniversidad de Buenos AiresBuenos AiresArgentina

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