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The antioxidant vitamin E modulates amyloid beta-peptide-induced creatine kinase activity inhibition and increased protein oxidation: implications for the free radical hypothesis of Alzheimer's disease.
Neurochem Res. 1999 Mar; 24(3):427-35.NR

Abstract

Amyloid beta-peptide (Abeta), the main constituent of senile plaques in Alzheimer's disease (AD) brain, is hypothesized to be a key factor in the neurodegeneration seen in AD. Recently it has been shown by us and others that the neurotoxicity of Abeta occurs in conjunction with free radical oxidative stress associated with the peptide. Abeta(1-40) and several other fragments of the Abeta sequence are associated with free radicals in solution that are detectable using electron paramagnetic resonance spectroscopy. These free radicals were shown to attack brain cell membranes, initiate lipid peroxidation, increase Ca2+ influx and damage membrane and cytosolic proteins. In AD brain obtained under rapid autopsy protocol, the activity of the oxidatively-sensitive enzyme creatine kinase was shown to be significantly reduced. We reasoned that Abeta-associated free radical-induced modification of creatine kinase activity and other markers of cellular damage might be modulated by free radical scavengers. Accordingly, this study demonstrates that vitamin E can modulate Abeta(25-35)-induced oxidative damage to creatine kinase and cellular proteins in cultured embryonic hippocampal neurons. These results, consistent with the hypothesis of free radical-mediated Abeta toxicity in AD, are discussed with deference to potential free radical scavengers as therapeutic agents for slowing the progression of AD.

Authors+Show Affiliations

Department of Chemistry and Center of Membrane Sciences, University of Kentucky Lexington, 40506-0055, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10215518

Citation

Yatin, S M., et al. "The Antioxidant Vitamin E Modulates Amyloid Beta-peptide-induced Creatine Kinase Activity Inhibition and Increased Protein Oxidation: Implications for the Free Radical Hypothesis of Alzheimer's Disease." Neurochemical Research, vol. 24, no. 3, 1999, pp. 427-35.
Yatin SM, Aksenov M, Butterfield DA. The antioxidant vitamin E modulates amyloid beta-peptide-induced creatine kinase activity inhibition and increased protein oxidation: implications for the free radical hypothesis of Alzheimer's disease. Neurochem Res. 1999;24(3):427-35.
Yatin, S. M., Aksenov, M., & Butterfield, D. A. (1999). The antioxidant vitamin E modulates amyloid beta-peptide-induced creatine kinase activity inhibition and increased protein oxidation: implications for the free radical hypothesis of Alzheimer's disease. Neurochemical Research, 24(3), 427-35.
Yatin SM, Aksenov M, Butterfield DA. The Antioxidant Vitamin E Modulates Amyloid Beta-peptide-induced Creatine Kinase Activity Inhibition and Increased Protein Oxidation: Implications for the Free Radical Hypothesis of Alzheimer's Disease. Neurochem Res. 1999;24(3):427-35. PubMed PMID: 10215518.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The antioxidant vitamin E modulates amyloid beta-peptide-induced creatine kinase activity inhibition and increased protein oxidation: implications for the free radical hypothesis of Alzheimer's disease. AU - Yatin,S M, AU - Aksenov,M, AU - Butterfield,D A, PY - 1999/4/24/pubmed PY - 1999/4/24/medline PY - 1999/4/24/entrez SP - 427 EP - 35 JF - Neurochemical research JO - Neurochem Res VL - 24 IS - 3 N2 - Amyloid beta-peptide (Abeta), the main constituent of senile plaques in Alzheimer's disease (AD) brain, is hypothesized to be a key factor in the neurodegeneration seen in AD. Recently it has been shown by us and others that the neurotoxicity of Abeta occurs in conjunction with free radical oxidative stress associated with the peptide. Abeta(1-40) and several other fragments of the Abeta sequence are associated with free radicals in solution that are detectable using electron paramagnetic resonance spectroscopy. These free radicals were shown to attack brain cell membranes, initiate lipid peroxidation, increase Ca2+ influx and damage membrane and cytosolic proteins. In AD brain obtained under rapid autopsy protocol, the activity of the oxidatively-sensitive enzyme creatine kinase was shown to be significantly reduced. We reasoned that Abeta-associated free radical-induced modification of creatine kinase activity and other markers of cellular damage might be modulated by free radical scavengers. Accordingly, this study demonstrates that vitamin E can modulate Abeta(25-35)-induced oxidative damage to creatine kinase and cellular proteins in cultured embryonic hippocampal neurons. These results, consistent with the hypothesis of free radical-mediated Abeta toxicity in AD, are discussed with deference to potential free radical scavengers as therapeutic agents for slowing the progression of AD. SN - 0364-3190 UR - https://www.unboundmedicine.com/medline/citation/10215518/The_antioxidant_vitamin_E_modulates_amyloid_beta_peptide_induced_creatine_kinase_activity_inhibition_and_increased_protein_oxidation:_implications_for_the_free_radical_hypothesis_of_Alzheimer's_disease_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=10215518.ui DB - PRIME DP - Unbound Medicine ER -