Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease.

Holsinger RM ¹,

McLean CA ,

Beyreuther K ,

Masters CL ,

Evin G

Affiliations

1. Department of Pathology, Mental Health Research Institute, The University of Melbourne, Parkville, Victoria 3010, Australia.
Authors
Holsinger RM¹
(1 author)

ORCIDs linked to this article

Annals of Neurology, 01 Jun 2002, 51(6):783-786
https://doi.org/10.1002/ana.10208 PMID: 12112088

Abstract

Beta-secretase cleavage represents the first step in the generation of Abeta polypeptides and initiates the amyloid cascade that leads to neurodegeneration in Alzheimer's disease. By comparative Western blot analysis, we show a 2.7-fold increase in protein expression of the beta-secretase enzyme BACE in the brain cortex of Alzheimer's disease patients as compared to age-matched controls. Similarly, we found the levels of the amyloid precursor protein C-terminal fragment produced by beta-secretase to be increased by nearly twofold in Alzheimer's disease cortex.

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Read article at publisher's site: https://doi.org/10.1002/ana.10208

References

Articles referenced by this article (19)

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Autoantibodies to BACE1 promote Aβ accumulation and neurodegeneration in Alzheimer's disease.
Wang YR, Zeng XQ, Wang J, Fowler CJ, Li QX, Bu XL, Doecke J, Maruff P, Martins RN, Rowe CC, Masters CL, Wang YJ, Liu YH
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This article is in the Europe PMC Open access subset. Refer to the copyright information in the article for licensing details.
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Inhibition of BACE1 affected both its Aβ producing and degrading activities and increased Aβ42 and Aβ40 levels at high-level BACE1 expression.
Ulku I, Leung R, Herre F, Walther L, Shobo A, Saftig P, Hancock MA, Liebsch F, Multhaup G
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Proteins in UniProt (Showing 5 of 13)

Beta-secretase 1(UniProt - B3KQJ4)
Beta-secretase 1(UniProt - Q8IYC8)
Peptidase A1 domain-containing protein(UniProt - B7Z3K2)
Beta-secretase 1(UniProt - P56817)
Peptidase A1 domain-containing protein(UniProt - Q5W9H2)

Go to all (13) records in UniProt

Search life-sciences literature (45,104,206 articles, preprints and more)

Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease.

Affiliations

ORCIDs linked to this article

Abstract

Full text links

References

Translating cell biology into therapeutic advances in Alzheimer's disease.

Abeta-generating enzymes: recent advances in beta- and gamma-secretase research.

Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE.

Purification and cloning of amyloid precursor protein beta-secretase from human brain.

Membrane-anchored aspartyl protease with Alzheimer's disease beta-secretase activity.

Identification of a novel aspartic protease (Asp 2) as beta-secretase.

Human aspartic protease memapsin 2 cleaves the beta-secretase site of beta-amyloid precursor protein.

Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation.

BACE1 is the major beta-secretase for generation of Abeta peptides by neurons.

BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics.

Citations & impact

Impact metrics

Citations of article over time

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Article citations

Autoantibodies to BACE1 promote Aβ accumulation and neurodegeneration in Alzheimer's disease.

Autophagy-lysosomal-associated neuronal death in neurodegenerative disease.

Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases.

Naringenin ameliorates amyloid-β pathology and neuroinflammation in Alzheimer's disease.

Inhibition of BACE1 affected both its Aβ producing and degrading activities and increased Aβ42 and Aβ40 levels at high-level BACE1 expression.

Data

Data that cites the article

Proteins in UniProt (Showing 5 of 13)

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Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease.

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