Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model - PubMed (original) (raw)

Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model

Jennifer Drake et al. Neurobiol Aging. 2003 May-Jun.

Abstract

Alzheimer's disease is a progressive, neurodegenerative disorder characterized by senile plaques and neurofibrillary components. Abeta(1-42) is a principal component of senile plaques and is thought to be central to the pathogenesis of the disease. The Alzheimer's disease brain is under significant oxidative stress, and the Abeta(1-42) peptide is known to cause oxidative stress in vitro. One controversy in the amyloid hypothesis is whether or not Abeta plaques are required for toxicity. We have employed a temperature-inducible Abeta expression system in Caenorhabditis elegans to create a strain of worms, CL4176, in which Abeta(1-42) is expressed with a non-permissive temperature of 23 degrees C. The CL4176 strain allows examination of the temporal relationship between Abeta expression, oxidative stress, and Abeta fibril formation. CL4176 were under increased oxidative stress, evidenced by increased protein oxidation indexed by increased carbonyl levels, 24 and 32 h after temperature upshift as compared to the control strain, CL1175. The increased oxidative stress in CL4176 occurred in the absence of Abeta fibril formation, consistent with the notion that the toxic species in Abeta toxicity is pre-fibrillar Abeta and not the Abeta fibril. These results are discussed with reference to Alzheimer's disease.

PubMed Disclaimer

Cited by

Beneficial Effects of Cyclic Ether 2-Butoxytetrahydrofuran from Sea Cucumber Holothuria scabra against Aβ Aggregate Toxicity in Transgenic Caenorhabditis elegans and Potential Chemical Interaction.
Tangrodchanapong T, Sornkaew N, Yurasakpong L, Niamnont N, Nantasenamat C, Sobhon P, Meemon K. Tangrodchanapong T, et al. Molecules. 2021 Apr 11;26(8):2195. doi: 10.3390/molecules26082195. Molecules. 2021. PMID: 33920352 Free PMC article.
Amyloid β-peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression.
Butterfield DA, Swomley AM, Sultana R. Butterfield DA, et al. Antioxid Redox Signal. 2013 Sep 10;19(8):823-35. doi: 10.1089/ars.2012.5027. Epub 2013 Feb 14. Antioxid Redox Signal. 2013. PMID: 23249141 Free PMC article. Review.
Jasonia glutinosa (L.) DC., a Traditional Herbal Tea, Exerts Antioxidant and Neuroprotective Properties in Different In Vitro and In Vivo Systems.
Les F, Valero MS, Moliner C, Weinkove D, López V, Gómez-Rincón C. Les F, et al. Biology (Basel). 2021 May 18;10(5):443. doi: 10.3390/biology10050443. Biology (Basel). 2021. PMID: 34069854 Free PMC article.
Redox proteomics in some age-related neurodegenerative disorders or models thereof.
Butterfield DA, Abdul HM, Newman S, Reed T. Butterfield DA, et al. NeuroRx. 2006 Jul;3(3):344-57. doi: 10.1016/j.nurx.2006.05.003. NeuroRx. 2006. PMID: 16815218 Free PMC article. Review.
Brain inflammation and oxidative stress in a transgenic mouse model of Alzheimer-like brain amyloidosis.
Yao Y, Chinnici C, Tang H, Trojanowski JQ, Lee VM, Praticò D. Yao Y, et al. J Neuroinflammation. 2004 Oct 22;1(1):21. doi: 10.1186/1742-2094-1-21. J Neuroinflammation. 2004. PMID: 15500684 Free PMC article.

Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model - PubMed (original) (raw)