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Abstract:

The deposition of 4-kDa amyloid β 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 β accumulates in the neuropil or within the walls of cerebral vessels, and associates with dementia or stroke, both hereditary and sporadic. Amyloid β 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 β levels may be achieved by inhibiting its generation from the amyloid β-precursor protein or by promoting its clearence by transport or degradation. We will summarize recent findings on brain proteases capable of degrading amyloid β 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 β in vivo. We will also put in perspective their possible utilization as therapeutic agents in amyloid β diseases.

Registro:

Documento: Artículo
Título:The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
Autor:Morelli, L.; Llovera, R.; Ibendahl, S.; Castaño, E.M.
Filiación:IQUIFIB, Departamento de Quimica Biologica, Universidad de Buenos Aires, Junín 956 CP 1113, Buenos Aires, Argentina
Palabras clave:Alzheimer disease; Amyloid β; Brain proteases; Cerebrovascular amyloidoses; Neurodegeneration; Therapy; amyloid beta protein; amyloid precursor protein; oligomer; Alzheimer disease; amyloid neuropathy; brain blood vessel; cerebrovascular disease; clinical feature; dementia; disease association; genetic disorder; human; molecular weight; neuropathology; neuropil; nonhuman; phenotype; priority journal; protein degradation; protein localization; protein transport; review; stroke; Alzheimer Disease; Amyloid beta-Protein; Amyloidosis; Brain; Endopeptidases; Humans; Hydrolysis
Año:2002
Volumen:27
Número:11
Página de inicio:1387
Página de fin:1399
DOI: http://dx.doi.org/10.1023/A:1021679817756
Título revista:Neurochemical Research
Título revista abreviado:Neurochem. Res.
ISSN:03643190
CODEN:NERED
CAS:amyloid beta protein, 109770-29-8; Amyloid beta-Protein; Endopeptidases, EC 3.4.-
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_03643190_v27_n11_p1387_Morelli

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Citas:

---------- APA ----------
Morelli, L., Llovera, R., Ibendahl, S. & Castaño, E.M. (2002) . The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses. Neurochemical Research, 27(11), 1387-1399.
http://dx.doi.org/10.1023/A:1021679817756
---------- CHICAGO ----------
Morelli, L., Llovera, R., Ibendahl, S., Castaño, E.M. "The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses" . Neurochemical Research 27, no. 11 (2002) : 1387-1399.
http://dx.doi.org/10.1023/A:1021679817756
---------- MLA ----------
Morelli, L., Llovera, R., Ibendahl, S., Castaño, E.M. "The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses" . Neurochemical Research, vol. 27, no. 11, 2002, pp. 1387-1399.
http://dx.doi.org/10.1023/A:1021679817756
---------- VANCOUVER ----------
Morelli, L., Llovera, R., Ibendahl, S., Castaño, E.M. The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses. Neurochem. Res. 2002;27(11):1387-1399.
http://dx.doi.org/10.1023/A:1021679817756