Home > Research > Publications & Outputs > Induction of cellular oxidative stress by the β...
View graph of relations

Induction of cellular oxidative stress by the β-amyloid peptide involved in Alzheimer's disease.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published

Standard

Induction of cellular oxidative stress by the β-amyloid peptide involved in Alzheimer's disease. / Gibson, G. L.; Allsop, David; Austen, B. M.
In: Protein and Peptide Letters, Vol. 11, No. 3, 2004, p. 257-270.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

APA

Vancouver

Author

Gibson, G. L. ; Allsop, David ; Austen, B. M. / Induction of cellular oxidative stress by the β-amyloid peptide involved in Alzheimer's disease. In: Protein and Peptide Letters. 2004 ; Vol. 11, No. 3. pp. 257-270.

Bibtex

@article{acbea611806c4eb6ac0504579b944458,
title = "Induction of cellular oxidative stress by the β-amyloid peptide involved in Alzheimer's disease.",
abstract = "β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.",
author = "Gibson, {G. L.} and David Allsop and Austen, {B. M.}",
year = "2004",
language = "English",
volume = "11",
pages = "257--270",
journal = "Protein and Peptide Letters",
issn = "0929-8665",
publisher = "Bentham Science Publishers B.V.",
number = "3",

}

RIS

TY - JOUR

T1 - Induction of cellular oxidative stress by the β-amyloid peptide involved in Alzheimer's disease.

AU - Gibson, G. L.

AU - Allsop, David

AU - Austen, B. M.

PY - 2004

Y1 - 2004

N2 - β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.

AB - β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.

M3 - Journal article

VL - 11

SP - 257

EP - 270

JO - Protein and Peptide Letters

JF - Protein and Peptide Letters

SN - 0929-8665

IS - 3

ER -