Mitochondrial dihydrolipoyl succinyltransferase deficiency accelerates amyloid pathology and memory deficit in a transgenic mouse model of amyloid deposition
- 1 October 2009
- journal article
- Published by Elsevier BV in Free Radical Biology & Medicine
- Vol. 47 (7), 1019-1027
- https://doi.org/10.1016/j.freeradbiomed.2009.07.008
Abstract
No abstract availableKeywords
This publication has 36 references indexed in Scilit:
- Thiamine deficiency induces oxidative stress and exacerbates the plaque pathology in Alzheimer's mouse modelNeurobiology of Aging, 2009
- Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout miceJournal of Neurochemistry, 2004
- Toxicity of Amyloid β Peptide: Tales of Calcium, Mitochondria, and Oxidative StressNeurochemical Research, 2004
- Gender differences in the amount and deposition of amyloidβ in APPswe and PS1 double transgenic miceNeurobiology of Disease, 2003
- Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of PathogenesisScience, 2003
- Lipid peroxidation and protein oxidation in Alzheimer’s disease brain: potential causes and consequences involving amyloid β-peptide-associated free radical oxidative stress1,2Free Radical Biology & Medicine, 2002
- Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid β-peptideTrends in Molecular Medicine, 2001
- Oxidative Damage Is the Earliest Event in Alzheimer DiseaseJournal of Neuropathology and Experimental Neurology, 2001
- Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer AmyloidosisJournal of Neuroscience, 2001
- Methionine residue 35 is important in amyloid β-peptide-associated free radical oxidative stressBrain Research Bulletin, 1999