The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses

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...

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Autores principales: Morelli, L., Llovera, R., Ibendahl, S., Castaño, E.M.
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_03643190_v27_n11_p1387_Morelli
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spelling todo:paper_03643190_v27_n11_p1387_Morelli2023-10-03T15:27:37Z The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses Morelli, L. Llovera, R. Ibendahl, S. Castaño, E.M. 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 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. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_03643190_v27_n11_p1387_Morelli
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic 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
spellingShingle 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
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
topic_facet 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
description 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.
format JOUR
author Morelli, L.
Llovera, R.
Ibendahl, S.
Castaño, E.M.
author_facet Morelli, L.
Llovera, R.
Ibendahl, S.
Castaño, E.M.
author_sort Morelli, L.
title The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
title_short The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
title_full The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
title_fullStr The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
title_full_unstemmed The degradation of amyloid β as a therapeutic strategy in Alzheimer's disease and cerebrovascular amyloidoses
title_sort degradation of amyloid β as a therapeutic strategy in alzheimer's disease and cerebrovascular amyloidoses
url http://hdl.handle.net/20.500.12110/paper_03643190_v27_n11_p1387_Morelli
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