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Chemical mechanism of Alzheimer's di...

Brunelle, Patrick.

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Chemical mechanism of Alzheimer's disease: Investigation of key reactions.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Chemical mechanism of Alzheimer's disease: Investigation of key reactions./
Author:	Brunelle, Patrick.
Description:	187 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4202.
Contained By:	Dissertation Abstracts International66-08B.
Subject:	Chemistry, Biochemistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR05626
ISBN:	9780494056264

Chemical mechanism of Alzheimer's disease: Investigation of key reactions.
Brunelle, Patrick.

Chemical mechanism of Alzheimer's disease: Investigation of key reactions. - 187 p.

Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4202.

Thesis (Ph.D.)--University of Calgary (Canada), 2005.

Alzheimer's disease is the most common cause of dementia among people 65 years of age and older. Over the last few years, using theoretical chemistry, we have developed a chemical model of Alzheimer's disease from numerous experimental observations. This thesis focuses on the investigation of the key steps in the chemical mechanism of Alzheimer's disease. First, the oxidation by Cu(II) of the lone methionine in Abeta, the peptide thought to cause Alzheimer's disease, was investigated. Three-electron bonding between the sulfur radical cation and biologically available electron lone pair donors gives reduction potentials in the range of 1.1 to 1.7 V. This places restrictions on the environment around the sulfur so that the reduction potential can be low enough to be oxidized by Cu(II). Secondly, the ability to transfer the radical damage from the oxidized sulfur to a more stable alphaC radical showed preference for two glycines (Gly29 and Gly33). Thirdly, the transfer from a alphaC protein-centered radical to an unsaturated lipid was demonstrated to be feasible when the protein is in an antiparallel beta-sheet. Finally, the effect of the lipid radical on the cell membrane is investigated by using the 1-palmitoyl-2-linoleyl-sn-glycero-phosphatidylcholine bilayer as a model. The bilayer model showed no effects on the bond dissociation free energies, but did display some interesting environmental effects on the unsaturated lipids around the radical. These environmental effects may have a significant consequence on the rate of lipid peroxidation in lipid bilayers. It is hoped that this research will provide further insights into the chemical mechanism of Azlheimer's disease, so that, one day, a cure or a way to prevent the disease can be found.

ISBN: 9780494056264Subjects--Topical Terms:

1017722
Chemistry, Biochemistry.

Chemical mechanism of Alzheimer's disease: Investigation of key reactions.
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520 $a Alzheimer's disease is the most common cause of dementia among people 65 years of age and older. Over the last few years, using theoretical chemistry, we have developed a chemical model of Alzheimer's disease from numerous experimental observations. This thesis focuses on the investigation of the key steps in the chemical mechanism of Alzheimer's disease. First, the oxidation by Cu(II) of the lone methionine in Abeta, the peptide thought to cause Alzheimer's disease, was investigated. Three-electron bonding between the sulfur radical cation and biologically available electron lone pair donors gives reduction potentials in the range of 1.1 to 1.7 V. This places restrictions on the environment around the sulfur so that the reduction potential can be low enough to be oxidized by Cu(II). Secondly, the ability to transfer the radical damage from the oxidized sulfur to a more stable alphaC radical showed preference for two glycines (Gly29 and Gly33). Thirdly, the transfer from a alphaC protein-centered radical to an unsaturated lipid was demonstrated to be feasible when the protein is in an antiparallel beta-sheet. Finally, the effect of the lipid radical on the cell membrane is investigated by using the 1-palmitoyl-2-linoleyl-sn-glycero-phosphatidylcholine bilayer as a model. The bilayer model showed no effects on the bond dissociation free energies, but did display some interesting environmental effects on the unsaturated lipids around the radical. These environmental effects may have a significant consequence on the rate of lipid peroxidation in lipid bilayers. It is hoped that this research will provide further insights into the chemical mechanism of Azlheimer's disease, so that, one day, a cure or a way to prevent the disease can be found.
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