Oxidative damage in brain from human mutant APP/PS-1 double knock-in mice as a function of age
- 16 August 2008
- journal article
- Published by Elsevier in Free Radical Biology & Medicine
- Vol. 45 (10), 1420-1425
- https://doi.org/10.1016/j.freeradbiomed.2008.08.012
Abstract
No abstract availableThis publication has 61 references indexed in Scilit:
- Roles of amyloid β-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairmentFree Radical Biology & Medicine, 2007
- Mutations in amyloid precursor protein and presenilin‐1 genes increase the basal oxidative stress in murine neuronal cells and lead to increased sensitivity to oxidative stress mediated by amyloid β‐peptide (1–42), H2O2 and kainic acid: implications for Alzheimer's diseaseJournal of Neurochemistry, 2006
- Free radicals and brain agingClinics in Geriatric Medicine, 2004
- DiscussionNeurobiology of Aging, 1999
- Mitochondrial Aging: Open QuestionsaAnnals of the New York Academy of Sciences, 1998
- Amyloid‐β Deposition in Alzheimer Transgenic Mice Is Associated with Oxidative StressJournal of Neurochemistry, 1998
- Processing of Alzheimer's Amyloid Precursor Protein during H2O2-Induced Apoptosis in Human Neuronal CellsBiochemical and Biophysical Research Communications, 1997
- Oxidative Stress Hypothesis in Alzheimer's DiseaseFree Radical Biology & Medicine, 1997
- Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In VivoNeuron, 1996
- Vitamin E protects nerve cells from amyloid βprotein toxicityBiochemical and Biophysical Research Communications, 1992