Channel formation in planar lipid bilayers by a neurotoxic fragment of the beta-amyloid peptide.
Channel formation in planar lipid bilayers by a neurotoxic fragment of the beta-amyloid peptide.
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DOI：
10.1006/bbrc.1994.2047
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发表时间：
1994-07
影响因子：
3.1
通讯作者：
T. Mirzabekov;Meng-Chin Lin;Weining Yuan;P. J. Marshall;M. Carman;K. Tomaselli;I. Lieberburg;B. Kagan
中科院分区：
文献类型：
--
作者：
T. Mirzabekov;Meng-Chin Lin;Weining Yuan;P. J. Marshall;M. Carman;K. Tomaselli;I. Lieberburg;B. Kagan
阿尔茨海默病（AD）病理学的特征在于斑块、缠结和神经元细胞损失。斑块的主要成分是β-淀粉样肽（A β），一种39-42个残基的肽，其与体外钙稳态破坏和神经毒性有关。我们证明，A β的神经毒性片段，A β（25-35）自发插入平面脂质膜，形成弱选择性，电压依赖性，离子渗透通道。提示AD的发病机制可能与通道形成有关，A β（25-35）可能是AD的活性通道形成片段。
Alzheimer's disease (AD) pathology is characterized by plaques, tangles, and neuronal cell loss. The main constituent of plaques is beta-amyloid peptide (A beta), a 39-42 residue peptide which has been linked to disruption of calcium homeostasis and neurotoxicity in vitro. We demonstrate that a neurotoxic fragment of A beta, A beta (25-35) spontaneously inserted into planar lipid membranes to form weakly selective, voltage dependent, ion-permeable channels. We suggest that channel formation may be involved in the pathogenesis of AD and that A beta (25-35) may be the active channel forming segment.