Shock membrane electropotential drops and limited diffusive distance of beta-amyloids in cerebral neurons are detrimental enhancement to Alzheimer's diseases.
Identifieur interne : 002007 ( PubMed/Corpus ); précédent : 002006; suivant : 002008Shock membrane electropotential drops and limited diffusive distance of beta-amyloids in cerebral neurons are detrimental enhancement to Alzheimer's diseases.
Auteurs : Chi-Huan Chang ; Chiung-Huei Peng ; Kuan-Chou Chen ; Hsien-Bin Huang ; Wen-Ta Chiu ; Robert Y. PengSource :
- Colloids and surfaces. B, Biointerfaces [ 1873-4367 ] ; 2009.
English descriptors
- KwdEn :
- Alzheimer Disease (physiopathology), Amyloid beta-Peptides (toxicity), Animals, Brain (drug effects), Brain (pathology), Calcium (metabolism), Chelating Agents (pharmacology), Diffusion, Electrolytes, Homeostasis (drug effects), Membrane Potentials (drug effects), Models, Biological, Neurons (drug effects), Neurons (pathology), Organ Specificity (drug effects), Time Factors, Viscosity (drug effects).
- MESH :
- chemical , metabolism : Calcium.
- chemical , pharmacology : Chelating Agents.
- chemical , toxicity : Amyloid beta-Peptides.
- drug effects : Brain, Homeostasis, Membrane Potentials, Neurons, Organ Specificity, Viscosity.
- pathology : Brain, Neurons.
- physiopathology : Alzheimer Disease.
- Animals, Diffusion, Electrolytes, Models, Biological, Time Factors.
Abstract
Molecular physicobiochemical calculations indicated that the metallic ion binding to beta-amyloids (Abeta) may induce production of hydrogen peroxide, which triggers the Ca ion redistribution from the extracellular to the intracellular compartmentation, resulting in a transient membrane electropotential drop by at least 208.06 mV. Moreover, using the Mark and Houwink empirical equation, we predicted that the diffusible distances of all Abeta identities would be confined in a very tiny region within a radius less than 3.96 x 10(-4)cm in brain at 192h after produced. Because of the inherent tendency of aggregation behaved by the Abetas, the maximum diffusion coefficient and inherent viscosity were 8.24 x 10(-15)cm(2)s(-1) and 72.15 cps for the 12 mers (40.8 kDa), the largest soluble form of ABs. Conclusively, we have quantitatively predicted that the shock membrane potential drop (Deltaphi>208.06 mV) and limited diffusible distance (<3.96 x 10(-4)cm) in the brain would contribute the major detrimental effects to the neurons in the Alzheimer's diseases.
DOI: 10.1016/j.colsurfb.2009.06.004
PubMed: 19574031
Links to Exploration step
pubmed:19574031Le document en format XML
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<author><name sortKey="Chang, Chi Huan" sort="Chang, Chi Huan" uniqKey="Chang C" first="Chi-Huan" last="Chang">Chi-Huan Chang</name>
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<author><name sortKey="Peng, Chiung Huei" sort="Peng, Chiung Huei" uniqKey="Peng C" first="Chiung-Huei" last="Peng">Chiung-Huei Peng</name>
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<author><name sortKey="Chen, Kuan Chou" sort="Chen, Kuan Chou" uniqKey="Chen K" first="Kuan-Chou" last="Chen">Kuan-Chou Chen</name>
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<author><name sortKey="Huang, Hsien Bin" sort="Huang, Hsien Bin" uniqKey="Huang H" first="Hsien-Bin" last="Huang">Hsien-Bin Huang</name>
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<author><name sortKey="Chiu, Wen Ta" sort="Chiu, Wen Ta" uniqKey="Chiu W" first="Wen-Ta" last="Chiu">Wen-Ta Chiu</name>
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<author><name sortKey="Peng, Robert Y" sort="Peng, Robert Y" uniqKey="Peng R" first="Robert Y" last="Peng">Robert Y. Peng</name>
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<author><name sortKey="Chiu, Wen Ta" sort="Chiu, Wen Ta" uniqKey="Chiu W" first="Wen-Ta" last="Chiu">Wen-Ta Chiu</name>
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<term>Brain (drug effects)</term>
<term>Brain (pathology)</term>
<term>Calcium (metabolism)</term>
<term>Chelating Agents (pharmacology)</term>
<term>Diffusion</term>
<term>Electrolytes</term>
<term>Homeostasis (drug effects)</term>
<term>Membrane Potentials (drug effects)</term>
<term>Models, Biological</term>
<term>Neurons (drug effects)</term>
<term>Neurons (pathology)</term>
<term>Organ Specificity (drug effects)</term>
<term>Time Factors</term>
<term>Viscosity (drug effects)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Amyloid beta-Peptides</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term>
<term>Homeostasis</term>
<term>Membrane Potentials</term>
<term>Neurons</term>
<term>Organ Specificity</term>
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<front><div type="abstract" xml:lang="en">Molecular physicobiochemical calculations indicated that the metallic ion binding to beta-amyloids (Abeta) may induce production of hydrogen peroxide, which triggers the Ca ion redistribution from the extracellular to the intracellular compartmentation, resulting in a transient membrane electropotential drop by at least 208.06 mV. Moreover, using the Mark and Houwink empirical equation, we predicted that the diffusible distances of all Abeta identities would be confined in a very tiny region within a radius less than 3.96 x 10(-4)cm in brain at 192h after produced. Because of the inherent tendency of aggregation behaved by the Abetas, the maximum diffusion coefficient and inherent viscosity were 8.24 x 10(-15)cm(2)s(-1) and 72.15 cps for the 12 mers (40.8 kDa), the largest soluble form of ABs. Conclusively, we have quantitatively predicted that the shock membrane potential drop (Deltaphi>208.06 mV) and limited diffusible distance (<3.96 x 10(-4)cm) in the brain would contribute the major detrimental effects to the neurons in the Alzheimer's diseases.</div>
</front>
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<DateRevised><Year>2013</Year>
<Month>11</Month>
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<Title>Colloids and surfaces. B, Biointerfaces</Title>
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<ArticleTitle>Shock membrane electropotential drops and limited diffusive distance of beta-amyloids in cerebral neurons are detrimental enhancement to Alzheimer's diseases.</ArticleTitle>
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<Abstract><AbstractText>Molecular physicobiochemical calculations indicated that the metallic ion binding to beta-amyloids (Abeta) may induce production of hydrogen peroxide, which triggers the Ca ion redistribution from the extracellular to the intracellular compartmentation, resulting in a transient membrane electropotential drop by at least 208.06 mV. Moreover, using the Mark and Houwink empirical equation, we predicted that the diffusible distances of all Abeta identities would be confined in a very tiny region within a radius less than 3.96 x 10(-4)cm in brain at 192h after produced. Because of the inherent tendency of aggregation behaved by the Abetas, the maximum diffusion coefficient and inherent viscosity were 8.24 x 10(-15)cm(2)s(-1) and 72.15 cps for the 12 mers (40.8 kDa), the largest soluble form of ABs. Conclusively, we have quantitatively predicted that the shock membrane potential drop (Deltaphi>208.06 mV) and limited diffusible distance (<3.96 x 10(-4)cm) in the brain would contribute the major detrimental effects to the neurons in the Alzheimer's diseases.</AbstractText>
</Abstract>
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<ForeName>Chi-Huan</ForeName>
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