Protein levels of human peroxiredoxin subtypes in brains of patients with Alzheimer's disease and Down syndrome
- PMID: 11771746
- DOI: 10.1007/978-3-7091-6262-0_18
Protein levels of human peroxiredoxin subtypes in brains of patients with Alzheimer's disease and Down syndrome
Abstract
Human peroxiredoxin (Prx) play important roles in eliminating hydrogen peroxide generated during cellular mechanisms using electrons from thioredoxin (Trx). Oxidative stress induced by reactive oxygen species (ROS) such as hydrogen peroxide has been implicated in the pathogenesis of several neurodegenerative diseases. We applied the proteomic approach to study protein levels of three subtypes of human Prx in brain regions from patients with Alzheimer's disease (AD) and Down Syndrome (DS). Protein levels of Prx-I and Prx-II were significantly increased in AD and DS. Protein levels of Prx-III, a mitochondrial protein, however, were significantly decreased. We conclude that increased protein levels of Prx-I and Prx-II could provide protection against neuronal cell death induced by hydrogen peroxide. Decreased protein levels of Prx-III could be caused by mitochondrial damage shown in AD and DS. Showing upregulated Prx protein levels provides evidence for the involvement of ROS in the pathogenesis of AD and DS.
Similar articles
-
Aberrant expression of peroxiredoxin subtypes in neurodegenerative disorders.Brain Res. 2003 Mar 28;967(1-2):152-60. doi: 10.1016/s0006-8993(02)04243-9. Brain Res. 2003. PMID: 12650976
-
Antioxidant proteins in fetal brain: superoxide dismutase-1 (SOD-1) protein is not overexpressed in fetal Down syndrome.J Neural Transm Suppl. 2001;(61):71-84. doi: 10.1007/978-3-7091-6262-0_6. J Neural Transm Suppl. 2001. PMID: 11771762
-
Decreased brain levels of 2',3'-cyclic nucleotide-3'-phosphodiesterase in Down syndrome and Alzheimer's disease.Neurobiol Aging. 2001 Jul-Aug;22(4):547-53. doi: 10.1016/s0197-4580(01)00218-4. Neurobiol Aging. 2001. PMID: 11445254
-
The thioredoxin antioxidant system.Free Radic Biol Med. 2014 Jan;66:75-87. doi: 10.1016/j.freeradbiomed.2013.07.036. Epub 2013 Jul 27. Free Radic Biol Med. 2014. PMID: 23899494 Review.
-
Peroxiredoxins, oxidative stress, and cell proliferation.Antioxid Redox Signal. 2005 May-Jun;7(5-6):768-77. doi: 10.1089/ars.2005.7.768. Antioxid Redox Signal. 2005. PMID: 15890023 Review.
Cited by
-
Lymphocyte mitochondria: toward identification of peripheral biomarkers in the progression of Alzheimer disease.Free Radic Biol Med. 2013 Dec;65:595-606. doi: 10.1016/j.freeradbiomed.2013.08.001. Epub 2013 Aug 8. Free Radic Biol Med. 2013. PMID: 23933528 Free PMC article.
-
Mitochondrial H2O2 as an enable signal for triggering autophosphorylation of insulin receptor in neurons.J Mol Signal. 2013 Oct 5;8(1):11. doi: 10.1186/1750-2187-8-11. J Mol Signal. 2013. PMID: 24094269 Free PMC article.
-
An investigation of the molecular mechanisms engaged before and after the development of Alzheimer disease neuropathology in Down syndrome: a proteomics approach.Free Radic Biol Med. 2014 Nov;76:89-95. doi: 10.1016/j.freeradbiomed.2014.08.006. Epub 2014 Aug 20. Free Radic Biol Med. 2014. PMID: 25151119 Free PMC article.
-
Age-related neurodegeneration and memory loss in down syndrome.Curr Gerontol Geriatr Res. 2012;2012:463909. doi: 10.1155/2012/463909. Epub 2012 Mar 20. Curr Gerontol Geriatr Res. 2012. PMID: 22545043 Free PMC article.
-
Longitudinal study of differential protein expression in an Alzheimer's mouse model lacking inducible nitric oxide synthase.J Proteome Res. 2013 Oct 4;12(10):4462-77. doi: 10.1021/pr4005103. Epub 2013 Sep 18. J Proteome Res. 2013. PMID: 24006891 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Medical
Molecular Biology Databases
Research Materials