Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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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 -