INVESTIGADORES
CASTAÑO Eduardo Miguel
artículos
Título:
The degradation of amyloid beta as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
Autor/es:
MORELLI L; LLOVERA R; IBENDHAL S; CASTAÑO EM
Revista:
NEUROCHEMICAL RESEARCH
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Lugar: New York; Año: 2002 vol. 27 p. 1387 - 1399
ISSN:
0364-3190
Resumen:
The deposition of 4-kDa amyloid beta peptide in the brain is a prominent
feature of several human diseases. Such process is heterogeneous in
terms of causative factors, biochemical phenotype, localization and
clinical manifestations. Amyloid beta accumulates in the neuropil or
within the walls of cerebral vessels, and associates with dementia or
stroke, both hereditary and sporadic. Amyloid beta is normally released
by cells as soluble monomeric-dimeric species yet, under pathological
conditions, it self-aggregates as soluble oligomers or insoluble fibrils
that may be toxic to neurons and vascular cells. Lowering amyloid beta
levels may be achieved by inhibiting its generation from the amyloid
beta-precursor protein or by promoting its clearance by transport or
degradation. We will summarize recent findings on brain proteases
capable of degrading amyloid beta with a special focus on those enzymes
for which there is genetic, transgenic or biochemical evidence
suggesting that they may participate in the proteolysis of amyloid beta
in vivo. We will also put in perspective their possible utilization as
therapeutic agents in amyloid beta diseases.