Seidler N W, Craig H D, Squire T J
Kansas City University of Medicine and Biosciences, Department of Biochemistry, 1750 Independence Avenue, Kansas City, MO 64106, USA.
Med Hypotheses. 2006;67(3):467-70. doi: 10.1016/j.mehy.2006.02.038. Epub 2006 May 6.
Accumulation of amyloid beta (Abeta) peptide in brain is the hallmark of Alzheimer's disease (AD). The resulting plaques though fibrous in nature may also consist of additional structures currently poorly defined. We hypothesize that plastic composite material contributes to plaque formation. This material is organized by polymers of acrolein, which is an oxidized lipid fragment found in AD. Acrolein, a 3-carbon compound, contains a carbonyl and a vinyl group that participate in polymerization via fundamental latex chemistry. The redox and surfactant properties of Abeta allow it to catalyze the polymerization of acrolein. We previously reported observations of thin plastic fragments of Abeta-polyacrolein. The current paper outlines the proposed steps in forming these plastic fragments. Endogenous plastic composite material may significantly contribute to the pathogenesis of AD.
淀粉样β（Aβ）肽在大脑中的积累是阿尔茨海默病（AD）的标志。由此产生的斑块虽然本质上是纤维状的，但也可能由目前定义不明确的其他结构组成。我们假设塑料复合材料有助于斑块的形成。这种材料由丙烯醛聚合物组成，丙烯醛是在AD中发现的一种氧化脂质片段。丙烯醛是一种三碳化合物，含有一个羰基和一个乙烯基，它们通过基本的乳胶化学参与聚合反应。Aβ的氧化还原和表面活性剂特性使其能够催化丙烯醛的聚合反应。我们之前报道过观察到Aβ-聚丙烯醛的薄塑料碎片。本文概述了形成这些塑料碎片的拟议步骤。内源性塑料复合材料可能对AD的发病机制有显著贡献。
