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Endogenous plastic composite material in the Alzheimer's brain.
N W Seidler1, H D Craig, T J Squire
1Kansas City University of Medicine and Biosciences, Department of Biochemistry, 1750 Independence Avenue, Kansas City, MO 64106, USA. nseidler@kcumb.edu
Medical Hypotheses
|May 9, 2006
Summary
Alzheimer's disease plaques may contain plastic composites formed by acrolein polymerization, catalyzed by amyloid beta. This endogenous material could significantly contribute to Alzheimer's pathogenesis.
Area of Science:
- Neuroscience
- Materials Science
- Biochemistry
Background:
- Alzheimer's disease (AD) is characterized by amyloid beta (Abeta) plaque accumulation in the brain.
- These plaques may contain poorly defined structures beyond fibrous amyloid beta.
Purpose of the Study:
- To investigate the hypothesis that plastic composite material contributes to Alzheimer's plaque formation.
- To elucidate the role of acrolein polymerization in the pathogenesis of AD.
Main Methods:
- Examining the chemical properties of acrolein, including its carbonyl and vinyl groups.
- Investigating the catalytic role of Abeta in acrolein polymerization using latex chemistry principles.
- Analyzing previously observed Abeta-polyacrolein plastic fragments.
Main Results:
- Acrolein, an oxidized lipid fragment, can polymerize via its functional groups.
- Abeta's redox and surfactant properties catalyze acrolein polymerization.
- Thin plastic fragments composed of Abeta-polyacrolein have been observed.
Conclusions:
- The formation of Abeta-polyacrolein plastic fragments is a proposed pathway in Alzheimer's pathogenesis.
- Endogenous plastic composite material may play a significant role in the development of Alzheimer's disease.